Updated on 2023/02/05

写真a

 
TADA Mari
 
Organization
Brain Research Institute Center for Bioresources Associate Professor
Title
Associate Professor
External link

Degree

  • 博士(医学) ( 2011.3   新潟大学 )

Research Interests

  • leukoencephalopathy

  • neurodegenerative disease

  • glia

  • neurology

  • neuropathology

Research Areas

  • Life Science / Anatomy and histopathology of nervous system  / neuropathology

  • Life Science / Neurology

  • Life Science / Psychiatry  / 認知症

Research History (researchmap)

  • Brain Research Institute, Niigata University   Department of Pathology   Associate Professor

    2019.7

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  • Niigata University   Brain Research Institute   Assistant Professor

    2012.5 - 2019.6

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  • Niigata University   Neurology, Medical and Dental Hospital

    2011.4 - 2012.4

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  • Niigata University   Brain Research Institute

    1997.4 - 2005.3

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Research History

  • Niigata University   Brain Research Institute Center for Bioresources   Associate Professor

    2019.7

  • Niigata University   Brain Research Institute Pathological Neuroscience Branch   Assistant Professor

    2012.5 - 2019.6

Education

  • Niigata University   Graduate School of Medical and Dental Sciences

    2005.4 - 2011.3

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Professional Memberships

Committee Memberships

  • 日本神経病理学会   代議員  

    2018.10   

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    Committee type:Academic society

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Papers

  • <i>SYNE1</i>-ataxia: clinicopathologic features of an autopsied patient with novel compound heterozygous mutations

    Rie Saito, Norikazu Hara, Mari Tada, Masatoshi Wakabayashi, Akinori Miyashita, Masatoyo Nishizawa, Osamu Onodera, Takeshi Ikeuchi, Akiyoshi Kakita

    Journal of Neuropathology &amp; Experimental Neurology   2022.12

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    Publishing type:Research paper (scientific journal)   Publisher:Oxford University Press (OUP)  

    DOI: 10.1093/jnen/nlac120

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  • Biallelic <i>COX10</i> Mutations and <i>PMP22</i> Deletion in a Family With Leigh Syndrome and Hereditary Neuropathy With Liability to Pressure Palsy

    Yasuko Kuroha, Takanobu Ishiguro, Mari Tada, Norikazu Hara, Kei Murayama, Izumi Kawachi, Kensaku Kasuga, Akinori Miyashita, Arika Hasegawa, Tetsuya Takahashi, Nae Matsubara, Osamu Onodera, Akiyoshi Kakita, Ryoko Koike, Takeshi Ikeuchi

    Neurology Genetics   8 ( 5 )   e200030 - e200030   2022.10

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    Publishing type:Research paper (scientific journal)   Publisher:Ovid Technologies (Wolters Kluwer Health)  

    Objectives

    Leigh syndrome is a progressive encephalopathy characterized by symmetrical lesions in brain. This study aimed to investigate the clinicopathologic and genetic characteristics of a family with Leigh syndrome and hereditary neuropathy with liability to pressure palsy (HNPP).

    Methods

    Data from a Japanese family's clinical features, MRIs, muscle biopsy, and an autopsy were analyzed. A whole-exome sequence was performed, as well as real-time PCR analysis to determine copy number variations and Western blot analyses.

    Results

    The proband and her 2 siblings developed spastic paraplegia and mental retardation during childhood. The proband and her sister had peripheral neuropathy, whereas their father developed compression neuropathy. Leigh encephalopathy was diagnosed neuropathologically. Brain MRI revealed changes in cerebral white matter as well as multiple lesions in the brainstem and cerebellum. Muscle biopsy revealed type 2 fiber uniformity and decreased staining of cytochrome c oxidase. The COX10 missense mutation was identified through whole-exome sequence. A 1.4-Mb genomic deletion extending from intron 5 of COX10 to PMP22 was detected.

    Discussion

    These findings suggest that in this family, Leigh syndrome is associated with a mitochondrial respiratory chain complex IV deficiency caused by biallelic COX10 mutations coexisting with HNPP caused by heterozygous PMP22 deletion.

    DOI: 10.1212/nxg.0000000000200030

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  • Pathological substrate of memory impairment in multiple system atrophy. International journal

    Yasuo Miki, Kunikazu Tanji, Kana Shinnai, Makoto T Tanaka, Firat Altay, Sandrine C Foti, Catherine Strand, Takanori Sasaki, Tomoya Kon, Shuji Shimoyama, Tomonori Furukawa, Haruo Nishijima, Hiromi Yamazaki, Yasmine T Asi, Conceição Bettencourt, Zane Jaunmuktane, Mari Tada, Fumiaki Mori, Hiroki Mizukami, Masahiko Tomiyama, Hilal A Lashuel, Tammaryn Lashley, Akiyoshi Kakita, Helen Ling, Andrew J Lees, Janice L Holton, Thomas T Warner, Koichi Wakabayashi

    Neuropathology and applied neurobiology   48 ( 7 )   e12844   2022.7

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    AIMS: Synaptic dysfunction in Parkinson's disease is caused by propagation of pathogenic α-synuclein between neurons. Previously, in multiple system atrophy (MSA), pathologically characterised by ectopic deposition of abnormal α-synuclein predominantly in oligodendrocytes, we demonstrated that the occurrence of memory impairment was associated with the number of α-synuclein-positive neuronal cytoplasmic inclusions (NCIs) in the hippocampus. In the present study, we aimed to investigate how abnormal α-synuclein in the hippocampus can lead to memory impairment. METHODS: We performed pathological and biochemical analyses using a mouse model of adult-onset MSA and human cases (MSA, N = 25; Parkinson's disease, N = 3; Alzheimer's disease, N = 2; normal controls, N = 11). In addition, the MSA model mice were examined behaviourally and physiologically. RESULTS: In the MSA model, inducible human α-synuclein was first expressed in oligodendrocytes and subsequently accumulated in the cytoplasm of excitatory hippocampal neurons (NCI-like structures) and their presynaptic nerve terminals with the development of memory impairment. α-Synuclein oligomers increased simultaneously in the hippocampus of the MSA model. Hippocampal dendritic spines also decreased in number, followed by suppression of long-term potentiation. Consistent with these findings obtained in the MSA model, post-mortem analysis of human MSA brain tissues showed that cases of MSA with memory impairment developed more NCIs in excitatory hippocampal neurons along with α-synuclein oligomers than those without. CONCLUSIONS: Our results provide new insights into the role of α-synuclein oligomers as a possible pathological cause of memory impairment in MSA.

    DOI: 10.1111/nan.12844

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  • Praja1 RING-finger E3 ubiquitin ligase is a common suppressor of neurodegenerative disease-associated protein aggregation. International journal

    Kazuhiko Watabe, Motoko Niida-Kawaguchi, Mari Tada, Yoichiro Kato, Makiko Murata, Kunikazu Tanji, Koichi Wakabayashi, Mitsunori Yamada, Akiyoshi Kakita, Noriyuki Shibata

    Neuropathology : official journal of the Japanese Society of Neuropathology   2022.6

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    The formation of misfolded protein aggregates is one of the pathological hallmarks of neurodegenerative diseases. We have previously demonstrated the cytoplasmic aggregate formation of adenovirally expressed transactivation response DNA-binding protein of 43 kDa (TDP-43), the main constituent of neuronal cytoplasmic aggregates in cases of amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD), in cultured neuronal cells under the condition of proteasome inhibition. The TDP-43 aggregate formation was markedly suppressed by co-infection of adenoviruses expressing heat shock transcription factor 1 (HSF1), a master regulator of heat shock response, and Praja1 RING-finger E3 ubiquitin ligase (PJA1) located downstream of the HSF1 pathway. In the present study, we examined other reportedly known E3 ubiquitin ligases for TDP-43, i.e. Parkin, RNF112 and RNF220, but failed to find their suppressive effects on neuronal cytoplasmic TDP-43 aggregate formation, although they all bind to TDP-43 as verified by co-immunoprecipitation. In contrast, PJA1 also binds to adenovirally expressed wild-type and mutated fused in sarcoma, superoxide dismutase 1, α-synuclein and ataxin-3, and huntingtin polyglutamine proteins in neuronal cultures and suppressed the aggregate formation of these proteins. These results suggest that PJA1 is a common sensing factor for aggregate-prone proteins to counteract their aggregation propensity, and could be a potential therapeutic target for neurodegenerative diseases that include ALS, FTLD, Parkinson's disease and polyglutamine diseases.

    DOI: 10.1111/neup.12840

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  • Endogenous human retrovirus-K is not increased in the affected tissues of Japanese ALS patients. International journal

    Tomohiko Ishihara, Akihide Koyama, Yuya Hatano, Ryoko Takeuchi, Yuka Koike, Taisuke Kato, Mari Tada, Akiyoshi Kakita, Osamu Onodera

    Neuroscience research   178   78 - 82   2022.2

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    Activation of human endogenous retrovirus-K (HERV-K) is one of the proposed risk factors for amyotrophic lateral sclerosis (ALS). The HERV-K envelope protein has been reported to show neurotoxicity, and development of therapy with reverse transcriptase inhibitors is being investigated. On the other hand, some reports have failed to show HERV-K activation in ALS. In this study, we analyzed the expression of HERV-K mRNA in the motor cortex and spinal cord of 15 Japanese patients with sporadic ALS and 19 controls using reverse transcriptase droplet digital PCR. This revealed no significant increase of HERV-K expression in ALS-affected tissues, suggesting that the association between ALS and HERV-K remains questionable.

    DOI: 10.1016/j.neures.2022.01.009

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  • Brain TDP-43 pathology in corticobasal degeneration: topographical correlation with neuronal loss. International journal

    Makoto Sainouchi, Mari Tada, Yusran Ady Fitrah, Norikazu Hara, Kou Tanaka, Jiro Idezuka, Izumi Aida, Takashi Nakajima, Akinori Miyashita, Kohei Akazawa, Takeshi Ikeuchi, Osamu Onodera, Akiyoshi Kakita

    Neuropathology and applied neurobiology   48 ( 3 )   e12786   2021.12

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    Authorship:Corresponding author   Language:English   Publishing type:Research paper (scientific journal)  

    AIMS: Neuronal and glial inclusions comprising transactive response DNA-binding protein of 43 kDa (TDP-43) have been identified in the brains of patients with corticobasal degeneration (CBD), and a possible correlation between the presence of these inclusions and clinical phenotypes has been speculated. However, the significance of TDP-43 pathology in the pathomechanism of CBD has remained unclear. Here we investigated the topographical relationship between TDP-43 inclusions and neuronal loss in CBD. METHODS: We estimated semi-quantitatively neuronal loss and TDP-43 pathology in the form of neuronal cytoplasmic inclusions (NCIs), astrocytic inclusions (AIs), oligodendroglial cytoplasmic inclusions (GCIs), and dystrophic neurites in 22 CNS regions in 10 patients with CBD. Then, the degree of correlation between the severity of neuronal loss and the quantity of each type of TDP-43 inclusion was assessed. We also investigated tau pathology in a similar manner. RESULTS: TDP-43 pathology was evident in 9 patients. The putamen and globus pallidus were the regions most frequently affected (80%). NCIs were the most prominent form, and their quantity was significantly correlated with the severity of neuronal loss in more than half of the regions examined. The quantities of TDP-43 NCIs and tau NCIs were correlated in only a few regions. The number of regions where the quantities of TDP-43 AIs and GCIs were correlated with the severity of neuronal loss was apparently small in comparison with that of NCIs. CONCLUSIONS: TDP-43 alterations in neurons, not closely associated with tau pathology, may be involved in the pathomechanism underlying neuronal loss in CBD.

    DOI: 10.1111/nan.12786

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  • Parkinson's disease and parkinsonism: Clinicopathological discrepancies on diagnosis in three patients. International journal

    Yasuko Toyoshima, Hitoshi Takahashi, Shinnichi Katada, Naoyuki Kojima, Mari Tada, Takashi Tani, Ryoko Koike, Takanori Nozawa, Izumi Aida, Takashi Nakajima, Osamu Onodera, Akiyoshi Kakita

    Neuropathology : official journal of the Japanese Society of Neuropathology   41 ( 6 )   450 - 456   2021.12

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    Parkinson's disease (PD) is one of the most common neurodegenerative disorders. The cardinal neuropathological features of PD include selective and progressive loss of pigmented neurons in the substantia nigra, deficiencies in dopaminergic signaling in the striatum, and occurrence of phosphorylated α-synuclein-identified Lewy bodies in the nervous system. Parkinsonism, the clinical presentation of movement disorders seen in PD, is a feature shared commonly by other pathologically distinct neurodegenerative diseases, such as progressive supranuclear palsy (PSP), corticobasal degeneration (CBD), and multiple system atrophy (MSA). Consequently, it is sometimes difficult to distinguish PD from such parkinsonism-related neurological disorders. In addition, parkinsonism is not always a feature of certain neurodegenerative diseases, and it can sometimes develop as a result of various forms of drug intoxication or cerebrovascular disease. Here, we describe the clinicopathological features of three patients (cases 1, 2, and 3) diagnosed as having PSP, MSA, and PD, respectively, in each of whom the postmortem histopathological diagnosis differed from the final clinical diagnosis. Neuropathologically, they had suffered from coexistent disorders: PD, MSA, and argyrophilic grain disease (case 1); PD (case 2); and vascular parkinsonism (case 3). The variety of patients showing features of parkinsonism underlines the importance of careful long-term follow up followed by postmortem neuropathological evaluation.

    DOI: 10.1111/neup.12777

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  • Alzheimer's Aβ assembly binds sodium pump and blocks endothelial NOS activity via ROS-PKC pathway in brain vascular endothelial cells. Reviewed International journal

    Tomoya Sasahara, Kaori Satomura, Mari Tada, Akiyoshi Kakita, Minako Hoshi

    iScience   24 ( 9 )   102936 - 102936   2021.9

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    Amyloid β-protein (Aβ) may contribute to worsening of Alzheimer's disease (AD) through vascular dysfunction, but the molecular mechanism involved is unknown. Using ex vivo blood vessels and primary endothelial cells from human brain microvessels, we show that patient-derived Aβ assemblies, termed amylospheroids (ASPD), exist on the microvascular surface in patients' brains and inhibit vasorelaxation through binding to the α3 subunit of sodium, potassium-ATPase (NAKα3) in caveolae on endothelial cells. Interestingly, NAKα3 is also the toxic target of ASPD in neurons. ASPD-NAKα3 interaction elicits neurodegeneration through calcium overload in neurons, while the same interaction suppresses vasorelaxation by increasing the inactive form of endothelial nitric oxide synthase (eNOS) in endothelial cells via mitochondrial ROS and protein kinase C, independently of the physiological relaxation system. Thus, ASPD may contribute to both neuronal and vascular pathologies through binding to NAKα3. Therefore, blocking the ASPD-NAKα3 interaction may be a useful target for AD therapy.

    DOI: 10.1016/j.isci.2021.102936

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  • Age-related demethylation of the TDP-43 autoregulatory region in the human motor cortex. Reviewed International journal

    Yuka Koike, Akihiro Sugai, Norikazu Hara, Junko Ito, Akio Yokoseki, Tomohiko Ishihara, Takuma Yamagishi, Shintaro Tsuboguchi, Mari Tada, Takeshi Ikeuchi, Akiyoshi Kakita, Osamu Onodera

    Communications biology   4 ( 1 )   1107 - 1107   2021.9

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    In amyotrophic lateral sclerosis (ALS), TAR DNA-binding protein 43 (TDP-43), which is encoded by TARDBP, forms aggregates in the motor cortex. This aggregate formation may be triggered by an increase in the TDP-43 level with aging. However, the amount of TDP-43 is autoregulated by alternative splicing of the TARDBP 3'UTR, and how this autoregulation is affected by aging remains to be elucidated. We found that DNA demethylation in the autoregulatory region in the TARDBP 3'UTR reduced alternative splicing and increased TARDBP mRNA expression. Furthermore, in the human motor cortex, we found that this region was demethylated with aging, resulting in increased expression of TARDBP mRNA. The acceleration of DNA demethylation in the motor cortex was associated with the age of ALS onset. In summary, the dysregulation of TDP-43 autoregulation by age-related DNA demethylation in the motor cortex may explain the contribution of aging and motor system selectivity in ALS.

    DOI: 10.1038/s42003-021-02621-0

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  • A novel splicing variant of ANXA11 in a patient with amyotrophic lateral sclerosis: histologic and biochemical features. Reviewed International journal

    Makoto Sainouchi, Yuya Hatano, Mari Tada, Tomohiko Ishihara, Shoichiro Ando, Taisuke Kato, Jun Tokunaga, Gaku Ito, Hiroaki Miyahara, Yasuko Toyoshima, Akio Yokoseki, Tetsutaro Ozawa, Kohei Akazawa, Osamu Onodera, Akiyoshi Kakita

    Acta neuropathologica communications   9 ( 1 )   106 - 106   2021.6

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    Authorship:Corresponding author   Language:English  

    DOI: 10.1186/s40478-021-01202-w

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  • 散発性ALSの137症例における剖検物のエキソーム分析(Exome analysis in 137 autopsied sporadic ALS cases)

    Ishihara Tomohiko, Hatano Yuya, Yokoseki Akio, Tada Mari, Nakajima Takashi, Koike Ryoko, Kakita Akiyoshi, Onodera Osamu

    臨床神経学   60 ( Suppl. )   S309 - S309   2020.11

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    Language:English   Publisher:(一社)日本神経学会  

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  • ALS剖検例に関するテキストマイニングとエキソーム分析を用いたALSの新規候補遺伝子の探索(Search for new candidate genes for ALS by textmining and exome analysis of autopsy cases)

    Hatano Yuya, Ishihara Tomohiko, Yokoseki Akio, Tada Mari, Kakita Akiyoshi, Okuda Shujiro, Onodera Osamu

    臨床神経学   60 ( Suppl. )   S324 - S324   2020.11

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  • Toward allele-specific targeting therapy and pharmacodynamic marker for spinocerebellar ataxia type 3. Reviewed International journal

    Mercedes Prudencio, Hector Garcia-Moreno, Karen R Jansen-West, Rana Hanna Al-Shaikh, Tania F Gendron, Michael G Heckman, Matthew R Spiegel, Yari Carlomagno, Lillian M Daughrity, Yuping Song, Judith A Dunmore, Natalie Byron, Björn Oskarsson, Katharine A Nicholson, Nathan P Staff, Sorina Gorcenco, Andreas Puschmann, João Lemos, Cristina Januário, Mark S LeDoux, Joseph H Friedman, James Polke, Robin Labrum, Vikram Shakkottai, Hayley S McLoughlin, Henry L Paulson, Takuya Konno, Osamu Onodera, Takeshi Ikeuchi, Mari Tada, Akiyoshi Kakita, John D Fryer, Christin Karremo, Inês Gomes, John N Caviness, Mark R Pittelkow, Jan Aasly, Ronald F Pfeiffer, Venka Veerappan, Eric R Eggenberger, William D Freeman, Josephine F Huang, Ryan J Uitti, Klaas J Wierenga, Iris V Marin Collazo, Philip W Tipton, Jay A van Gerpen, Marka van Blitterswijk, Guojun Bu, Zbigniew K Wszolek, Paola Giunti, Leonard Petrucelli

    Science translational medicine   12 ( 566 )   2020.10

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    Spinocerebellar ataxia type 3 (SCA3), caused by a CAG repeat expansion in the ataxin-3 gene (ATXN3), is characterized by neuronal polyglutamine (polyQ) ATXN3 protein aggregates. Although there is no cure for SCA3, gene-silencing approaches to reduce toxic polyQ ATXN3 showed promise in preclinical models. However, a major limitation in translating putative treatments for this rare disease to the clinic is the lack of pharmacodynamic markers for use in clinical trials. Here, we developed an immunoassay that readily detects polyQ ATXN3 proteins in human biological fluids and discriminates patients with SCA3 from healthy controls and individuals with other ataxias. We show that polyQ ATXN3 serves as a marker of target engagement in human fibroblasts, which may bode well for its use in clinical trials. Last, we identified a single-nucleotide polymorphism that strongly associates with the expanded allele, thus providing an exciting drug target to abrogate detrimental events initiated by mutant ATXN3. Gene-silencing strategies for several repeat diseases are well under way, and our results are expected to improve clinical trial preparedness for SCA3 therapies.

    DOI: 10.1126/scitranslmed.abb7086

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  • Novel CHP1 mutation in autosomal-recessive cerebellar ataxia: autopsy features of two siblings. Reviewed International journal

    Rie Saito, Norikazu Hara, Mari Tada, Yoshiaki Honma, Akinori Miyashita, Osamu Onodera, Takeshi Ikeuchi, Akiyoshi Kakita

    Acta neuropathologica communications   8 ( 1 )   134 - 134   2020.8

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    DOI: 10.1186/s40478-020-01008-2

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  • Praja1 RING-finger E3 ubiquitin ligase suppresses neuronal cytoplasmic TDP-43 aggregate formation. Reviewed International journal

    Kazuhiko Watabe, Yoichiro Kato, Miho Sakuma, Makiko Murata, Motoko Niida-Kawaguchi, Taro Takemura, Nobutaka Hanagata, Mari Tada, Akiyoshi Kakita, Noriyuki Shibata

    Neuropathology : official journal of the Japanese Society of Neuropathology   40 ( 6 )   570 - 586   2020.7

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    Transactivation response DNA-binding protein of 43 kDa (TDP-43) is a major constituent of cytoplasmic aggregates in neuronal and glial cells in cases of amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD). We have previously shown neuronal cytoplasmic aggregate formation induced by recombinant adenoviruses expressing human wild-type and C-terminal fragment (CTF) TDP-43 under the condition of proteasome inhibition in vitro and in vivo. In the present study, we demonstrated that the formation of the adenoviral TDP-43 aggregates was markedly suppressed in rat neural stem cell-derived neuronal cells by co-infection of an adenovirus expressing heat shock transcription factor 1 (HSF1), a master regulator of heat shock response. We performed DNA microarray analysis and searched several candidate molecules, located downstream of HSF1, which counteract TDP-43 aggregate formation. Among these, we identified Praja 1 RING-finger E3 ubiquitin ligase (PJA1) as a suppressor of phosphorylation and aggregate formation of TDP-43. Co-immunoprecipitation assay revealed that PJA1 binds to CTF TDP-43 and the E2-conjugating enzyme UBE2E3. PJA1 also suppressed formation of cytoplasmic phosphorylated TDP-43 aggregates in mouse facial motor neurons in vivo. Furthermore, phosphorylated TDP-43 aggregates were detected in PJA1-immunoreactive human ALS motor neurons. These results indicate that PJA1 is one of the principal E3 ubiquitin ligases for TDP-43 to counteract its aggregation propensity and could be a potential therapeutic target for ALS and FTLD.

    DOI: 10.1111/neup.12694

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  • TAF15が主要に蓄積したFET病理を伴う筋萎縮性側索硬化症 剖検例の臨床病理学的特徴(Amsotrophic lateral sclerosis with TAF15-predominant FET pathology: clinicopathologic features of an autopsied patient)

    Cui Bo, Tada Mari, Hatano Yuya, Takeshima Akari, Ishihara Tomohiko, Sugai Akihiro, Tokutake Takayoshi, Kanazawa Masato, Onodera Osamu, Kakita Akiyoshi

    新潟医学会雑誌   133 ( 11-12 )   391 - 391   2019.12

  • Phosphorylated TDP-43 aggregates in skeletal and cardiac muscle are a marker of myogenic degeneration in amyotrophic lateral sclerosis and various conditions. Reviewed

    Mori F, Tada M, Kon T, Miki Y, Tanji K, Kurotaki H, Tomiyama M, Ishihara T, Onodera O, Kakita A, Wakabayashi K

    Acta neuropathologica communications   7 ( 1 )   165   2019.10

  • TDP-43 プロテイノパチー (1) 前頭側頭葉変性症 (FTLD) Invited

    他田 真理, 柿田 明美

    病理と臨床   37 ( 9 )   2019.9

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    連載 –変性疾患のみかた–

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  • Clinicopathologic Features of Two Patients With Sporadic Amyotrophic Lateral Sclerosis Who Maintained Communication Ability for Over 30 Years. Reviewed International journal

    Junko Ito, Tetsuro Shimada, Mari Tada, Hiroshi Shimizu, Masatoshi Wakabayashi, Akio Yokoseki, Osamu Onodera, Hitoshi Takahashi, Akiyoshi Kakita

    Journal of neuropathology and experimental neurology   77 ( 11 )   981 - 986   2018.11

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    We report the clinicopathologic features of 2 unrelated patients with sporadic amyotrophic lateral sclerosis (SALS) supported by tracheostomy and invasive ventilation (TIV) who were able to maintain communication ability for more than 30 years after disease onset. In both cases, the age at onset was younger than the mean, initially the progression of muscle weakness was consistent with that in the majority of SALS patients, and TIV became necessary several years after disease onset. Thereafter, however, their neurologic deterioration slowed and the patients were able to operate computers by facial movements for several decades. At autopsy, neuronal loss appeared to be confined to the motor neuron system. Furthermore, while Betz cells and lower motor neurons in the spinal anterior horns and hypoglossal nucleus were severely depleted, other pyramidal neurons in the motor cortex, and lower motor neurons in the other brainstem motor nuclei were retained. Neuronal and glial cytoplasmic inclusions immunoreactive for phosphorylated 43-kDa TAR DNA-binding protein (TDP-43) were evident in the CNS, but in extremely small numbers. The present patients may represent a distinct subgroup of patients with SALS who are able to maintain communication ability for an extremely long period, accompanied by very mild TDP-43 pathology.

    DOI: 10.1093/jnen/nly082

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  • Neuronal intranuclear inclusion disease showing intranuclear inclusions in renal biopsy 12 years earlier. Reviewed International journal

    Motoki M, Nakajima H, Sato T, Tada M, Kakita A, Arawaka S

    Neurology   91 ( 19 )   884 - 886   2018.10

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    DOI: 10.1212/WNL.0000000000006480

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  • Altered expression of glutamate transporter-1 and water channel protein aquaporin-4 in human temporal cortex with Alzheimer's disease. Reviewed

    Hoshi A, Tsunoda A, Yamamoto T, Tada M, Kakita A, Ugawa Y

    Neuropathology and applied neurobiology   44 ( 6 )   628 - 638   2018.10

  • Vertical Gaze Palsy Caused by Selective Unilateral Rostral Midbrain Infarction. Reviewed International journal

    Misato Yokose, Kohei Furuya, Masayuki Suzuki, Tadashi Ozawa, Younhee Kim, Kumiko Miura, Kosuke Matsuzono, Takafumi Mashiko, Mari Tada, Reiji Koide, Haruo Shimazaki, Tohru Matsuura, Shigeru Fujimoto

    Neuro-ophthalmology (Aeolus Press)   42 ( 5 )   309 - 311   2018.10

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    Vertical gaze palsy is rarely a neurological symptom, although it has been observed in some cases. Here, we report the case of a patient presenting with complete upward and downward gaze palsy. In this case, a small lesion in the left rostral midbrain was observed on diffusion-weighted magnetic resonance (MR) images, and the lesion was considered to cause the ocular symptom. We consider that vertical gaze palsy is an important clue to an accurate topical diagnosis of a brain lesion.

    DOI: 10.1080/01658107.2017.1401092

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  • Loss of Motor Neurons Innervating Cervical Muscles in Patients With Multiple System Atrophy and Dropped Head. Reviewed International journal

    Rie Saito, Mari Tada, Yasuko Toyoshima, Masatoyo Nishizawa, Osamu Onodera, Hitoshi Takahashi, Akiyoshi Kakita

    Journal of neuropathology and experimental neurology   77 ( 4 )   317 - 324   2018.4

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    We investigated whether loss of motor neurons innervating the neck muscles contributes to dropped head (DH) in multiple system atrophy (MSA). From 75 patients with autopsy-proven MSA, we retrieved 3 who had DH (MSA-DH), and examined the 4th cervical cord segments. Neurons of the medial and lateral nuclear groups (MNG and LNG) innervate the neck and shoulder muscles, respectively. We measured the area of individual neurons in the MNG and LNG, and created an area-frequency histogram. Neurons were classified as large or small based on their area, and their total numbers in the MNG and LNG were counted. In the MNG, the numbers of both total neurons and large neurons were significantly lower in MSA patients than in the controls (214.2 ± 91.4 vs 521.3 ± 74.8, p = 0.0030, and 26.2 ± 9.1 vs 88.0 ± 34.6, p = 0.020, respectively), and were significantly lower in MSA-DH than in MSA-nonDH (139.7 ± 7.6 vs 288.7 ± 74.6, p = 0.048, and 18.0 ± 4.1 vs 34.3 ± 4.1, p = 0.016, respectively). There were no differences in the LNG neuron counts between the MSA-DH and MSA-nonDH groups. Loss of cervical motor neurons may be responsible for DH in MSA.

    DOI: 10.1093/jnen/nly007

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  • 常染色体劣性遺伝性が疑われる若年発症 緩徐進行性小脳失調症の1剖検例

    齋藤 理恵, 他田 真理, 若林 允甫, 小野寺 理, 高橋 均, 池内 健, 柿田 明美, 横尾 英明

    信州医学雑誌   66 ( 1 )   111 - 112   2018.2

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  • The SMN gene copy number states in Japanese ALS patients

    Ishihara T, Toyoda S, Koyama A, Tada M, Atsuta N, Nakamura R, Tohnai G, Sone J, Izumi Y, Kaji R, Morita M, Taniguchi A, Kakita A, Sobue G, Nishizawa M, Onodera O

    JOURNAL OF THE NEUROLOGICAL SCIENCES   381   211-211   2017.10

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  • Diagnostic criteria for adult-onset leukoencephalopathy with axonal spheroids and pigmented glia due to CSF1R mutation. Reviewed

    T Konno, K Yoshida, I Mizuta, T Mizuno, Toshitaka Kawarai, M Tada, H Nozaki, S-I Ikeda, O Onodera, K Z Wszolek, T Ikeuchi

    European Journal of Neurology   Vol.25 ( No.1 )   142 - 147   2017.9

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    These diagnostic criteria are very sensitive for diagnosing ALSP with sufficient specificity for differentiation from CADASIL and moderate specificity for other leukoencephalopathies. Our results suggest that these criteria are useful for the clinical diagnosis of ALSP.

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  • Expression of Aquaporin 1 and Aquaporin 4 in the Temporal Neocortex of Patients with Parkinson's Disease Reviewed

    Akihiko Hoshi, Ayako Tsunoda, Mari Tada, Masatoyo Nishizawa, Yoshikazu Ugawa, Akiyoshi Kakita

    BRAIN PATHOLOGY   27 ( 2 )   160 - 168   2017.3

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    The astrocytic water channel proteins aquaporin 1 (AQP1) and aquaporin 4 (AQP4) are known to be altered in brains affected by several neurodegenerative disorders, including Alzheimer's disease. However, AQP expression in brains affected by Parkinson's disease (PD) has not been described in detail. Recently, it has been reported that alpha-synuclein (alpha-syn)-immunolabeled astrocytes show preferential distribution in several cerebral regions, including the neocortex, in patients with PD. Here, we investigated whether AQP expression is associated with alpha-syn deposition in the temporal neocortex of PD patients. In accordance with the consensus criteria for dementia with Lewy bodies, the patients were classified into neocortical (PDneo), limbic (PDlim), and brain stem (PDbs) groups. Expressions of alpha-syn, AQP1, and AQP4 in the temporal lobes of the individual PD patients were examined immunohistochemically. Immunohistochemical analysis demonstrated more numerous AQP4-positive and AQP1-positive astrocytes in the PDneo group than in the PDbs, PDlim, and control groups. However, in the PDneo cases, these astrocytes were not often observed in alpha-syn-rich areas, and semiquantitative analysis revealed that there was a significant negative correlation between the levels of AQP4 and alpha-syn in layers V-VI, and between those of AQP1 and alpha-syn in layers II-III. These findings suggest that a defined population of AQP4- and AQP1-expressing reactive astrocytes may modify alpha-syn deposition in the neocortex of patients with PD.

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  • Characteristic Microglial Features in Patients with Hereditary Diffuse Leukoencephalopathy with Spheroids Reviewed

    Mari Tada, Takuya Konno, Masayoshi Tada, Toshiyuki Tezuka, Takeshi Miura, Naomi Mezaki, Ken-ichi Okazaki, Musashi Arakawa, Kyoko Itoh, Toru Yamamoto, Hideaki Yokoo, Nobuaki Yoshikura, Kenji Ishihara, Masao Horie, Hirohide Takebayashi, Yasuko Toyoshima, Makoto Naito, Osamu Onodera, Masatoyo Nishizawa, Hitoshi Takahashi, Takeshi Ikeuchi, Akiyoshi Kakita

    ANNALS OF NEUROLOGY   80 ( 4 )   554 - 565   2016.10

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    Objective: To clarify the histopathological alterations of microglia in the brains of patients with hereditary diffuse leukoencephalopathy with spheroids (HDLS) caused by mutations of the gene encoding the colony stimulating factor-1 receptor (CSF-1R).
    Methods: We examined 5 autopsied brains and 1 biopsy specimen from a total of 6 patients with CSF-1R mutations. Detailed immunohistochemical, biochemical, and ultrastructural features of microglia were examined, and quantitative analyses were performed.
    Results: In layers 3 to 4 of the frontal cortex in HDLS brains, microglia showed relatively uniform and delicate morphology, with thin and winding processes accompanying knotlike structures, and significantly smaller areas of Iba1 immunoreactivity and lower numbers of Iba1-positive cells were evident in comparison with control brains. On the other hand, in layers 5 to 6 and the underlying white matter, microglia were distributed unevenly; that is, in some areas they had accumulated densely, whereas in others they were scattered. Immunoblot analyses of microglia-associated proteins, including CD11b and DAP12, revealed that HDLS brains had significantly lower amounts of these proteins than diseased controls, although Ki-67-positive proliferative microglia were not reduced. Ultrastructurally, the microglial cytoplasm and processes in HDLS showed vesiculation of the rough endoplasmic reticulum and disaggregated polyribosomes, indicating depression of protein synthesis. On the other hand, macrophages were immunonegative for GLUT-5 or P2ry12, indicating that they were derived from bone marrow.
    Interpretation: The pathogenesis of HDLS seems to be associated with microglial vulnerability and morphological alterations.

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  • Increased neuronal and astroglial aquaporin-1 immunoreactivity in rat striatum by chemical preconditioning with 3-nitropropionic acid Reviewed

    Akihiko Hoshi, Ayako Tsunoda, Teiji Yamamoto, Mari Tada, Akiyoshi Kakita, Yoshikazu Ugawa

    NEUROSCIENCE LETTERS   626   48 - 53   2016.7

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    Aquaporin-1 (AQPI) is a water channel expressed in the choroid plexus and participates in forming cerebrospinal fluid. Interestingly, reactive astrocytes also express AQPI in the central nervous system under some pathological conditions. On the other hand, 3-nitropropionic acid (3NP) is a mitochondrial toxin that causes selective degeneration of striatum; however, its chemical preconditioning is neuroprotective against cerebral ischemia. We previously reported that mild 3NP application is accompanied with numerous reactive astrocytes in rat striatum devoid of typical necrotic lesions. Therefore, we studied whether AQPI in the rat striatum could be upregulated with reactive astrocytosis using the 3NP model. Immunohistochemical or immunofluorescence analysis showed that reactive astrocytosis in the striatum, which upregulates glial fibrillary acidic protein and glutamine synthetase, was induced by mild doses of 3NP administration. Intriguingly, after 3NP treatment, AQPI was intensely expressed not only by the subpopulation of astroglia but also by neurons. The AQPI immunoreactivity became more intensified at the early-subtoxic stage (ES: 24-48 h), but not as much in the delayed-subtoxic stage (DS: 96-120 h). In contrast, AQP4 expression in the striatum was downregulated after 3NP treatment, in particular during the ES stage. AQPI upregulation/AQP4 downregulation induced under subtoxic 3NP treatment may play a pivotal role in water homeostasis and cell viability in the striatum. (C) 2016 Elsevier Ireland Ltd. All rights reserved.

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  • Heterogeneity of cerebral TDP-43 pathology in sporadic amyotrophic lateral sclerosis: Evidence for clinico-pathologic subtypes Reviewed

    Ryoko Takeuchi, Mari Tada, Atsushi Shiga, Yasuko Toyoshima, Takuya Konno, Tomoe Sato, Hiroaki Nozaki, Taisuke Kato, Masao Horie, Hiroshi Shimizu, Hirohide Takebayashi, Osamu Onodera, Masatoyo Nishizawa, Akiyoshi Kakita, Hitoshi Takahashi

    ACTA NEUROPATHOLOGICA COMMUNICATIONS   4 ( 1 )   61   2016.6

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    Frontotemporal lobar degeneration (FTLD) and amyotrophic lateral sclerosis (ALS) are types of major TDP-43 (43-kDa TAR DNA-binding protein) proteinopathy. Cortical TDP-43 pathology has been analyzed in detail in cases of FTLD-TDP, but is still unclear in cases of ALS. We attempted to clarify the cortical and subcortical TDP-43 pathology in Japanese cases of sporadic ALS (n = 96) using an antibody specific to phosphorylated TDP-43 (pTDP-43). The cases were divided into two groups: those without pTDP-43-positive neuronal cytoplasmic inclusions in the hippocampal dentate granule cells (Type 1, n = 63), and those with such inclusions (Type 2, n = 33). Furthermore, the Type 2 cases were divided into two subgroups based on semi-quantitative estimation of pTDP-43-positive dystrophic neurites (DNs) in the temporal neocortex: Type 2a (accompanied by no or few DNs, n = 22) and Type 2b (accompanied by abundant DNs, n = 11). Clinico-pathologic analysis revealed that cognitive impairment was a feature in patients with Type 2a and Type 2b, but not in those with Type 1, and that importantly, Type 2b is a distinct subtype characterized by a poor prognosis despite the less severe loss of lower motor neurons, the unusual subcortical dendrospinal pTDP-43 pathology, and more prominent glial involvement in cortical pTDP-43 pathology than other two groups. Considering the patient survival time and severity of motor neuron loss in each group, transition from Type 1 to Type 2, or from Type 2a to Type 2b during the disease course appeared unlikely. Therefore, each of these three groups was regarded as an independent subtype.

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  • Pathological and Clinical Spectrum of Progressive Supranuclear Palsy: With Special Reference to Astrocytic Tau Pathology Reviewed

    Yuichi Yokoyama, Yasuko Toyoshima, Atsushi Shiga, Mari Tada, Hideaki Kitamura, Kazuko Hasegawa, Osamu Onodera, Takeshi Ikeuchi, Toshiyuki Someya, Masatoyo Nishizawa, Akiyoshi Kakita, Hitoshi Takahashi

    BRAIN PATHOLOGY   26 ( 2 )   155 - 166   2016.3

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    Progressive supranuclear palsy (PSP) is a four-repeat tauopathy with tau-positive, argyrophilic tuft-shaped astrocytes (TAs). We performed a pathological and clinical investigation in 40 consecutive autopsied Japanese patients with pathological diagnoses of PSP or PSP-like disease. Unequivocal TAs were present in 22 cases, all of which were confirmed to be PSP. Such TAs were hardly detected in the other 18 cases, which instead exhibited tau-positive, argyrophilic astrocytes, appearing as comparatively small clusters with central nuclei of irregularly shaped, coarse structures (equivocal TAs). Cluster analysis of the distribution pattern of tau-related pathology for these 18 cases identified two subgroups, pallido-nigro-luysian atrophy (PNLA) Type 1 (n=9) and Type 2 (n=9), the former being distinguished from the latter by the presence of tau-related lesions in the motor cortex, pontine nucleus and cerebellar dentate nucleus in addition to the severely affected PNL system. The duration from symptom onset until becoming wheelchair-bound was significantly longer in PNLAType 1. Immunoblotting of samples from the three disease conditions revealed band patterns of low-molecular-mass tau fragments at approximate to 35kDa. These findings shed further light on the wide pathological and clinical spectrum of four-repeat tauopathy, representing PSP in the broad sense rather than classical PSP.

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  • Globular Glial Mixed Four Repeat Tau and TDP-43 Proteinopathy with Motor Neuron Disease and Frontotemporal Dementia. Reviewed

    Takeuchi R, Toyoshima Y, Tada M, Tanaka H, Shimizu H, Shiga A, Miura T, Aoki K, Aikawa A, Ishizawa S, Ikeuchi T, Nishizawa M, Kakita A, Takahashi H

    Brain Pathology   26 ( 1 )   82 - 94   2016.1

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  • Globular Glial Mixed Four Repeat Tau and TDP-43 Proteinopathy with Motor Neuron Disease and Frontotemporal Dementia Reviewed

    Ryoko Takeuchi, Yasuko Toyoshima, Mari Tada, Hidetomo Tanaka, Hiroshi Shimizu, Atsushi Shiga, Takeshi Miura, Kenju Aoki, Akane Aikawa, Shin Ishizawa, Takeshi Ikeuchi, Masatoyo Nishizawa, Akiyoshi Kakita, Hitoshi Takahashi

    BRAIN PATHOLOGY   26 ( 1 )   82 - 94   2016.1

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    Amyotrophic lateral sclerosis (ALS) may be accompanied by frontotemporal dementia (FTD). We report a case of glial mixed tau and TDP-43 proteinopathies in a Japanese patient diagnosed clinically as having ALS-D. Autopsy revealed loss of lower motor neurons and degeneration of the pyramidal tracts in the spinal cord and brain stem. The brain showed frontotemporal lobar degeneration (FTLD), the most severe neuronal loss and gliosis being evident in the precentral gyrus. Although less severe, such changes were also observed in other brain regions, including the basal ganglia and substantia nigra. AT8 immunostaining revealed that predominant occurrence of astrocytic tau lesions termed globular astrocytic inclusions (GAIs) was a feature of the affected regions. These GAIs were Gallyas-Braak negative. Neuronal and oligodendrocytic tau lesions were comparatively scarce. pS409/410 immunostaining also revealed similar neuronal and glial TDP-43 lesions. Interestingly, occasional co-localization of tau and TDP-43 was evident in the GAIs. Immunoblot analyses revealed band patterns characteristic of a 4-repeat (4R) tauopathy, corticobasal degeneration and a TDP-43 proteinopathy, ALS/FTLD-TDPTypeB. No mutations were found in the MAPT or TDP-43 genes. We consider that this patient harbored a distinct, sporadic globular glial mixed 4R tau and TDP-43 proteinopathy associated with motor neuron disease and FTD.

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  • Na, K-ATPase alpha 3 is a death target of Alzheimer patient amyloid-beta assembly Reviewed

    Takayuki Ohnishi, Masako Yanazawa, Tomoya Sasahara, Yasuki Kitamura, Hidekazu Hiroaki, Yugo Fukazawa, Isao Kii, Takashi Nishiyama, Akiyoshi Kakita, Hiroyuki Takeda, Akihide Takeuchi, Yoshie Arai, Akane Ito, Hitomi Komura, Hajime Hirao, Kaori Satomura, Masafumi Inoue, Shin-ichi Muramatsu, Ko Matsui, Mari Tada, Michio Sato, Eri Saijo, Yoshiki Shigemitsu, Satoko Sakai, Yoshitaka Umetsu, Natsuko Goda, Naomi Takino, Hitoshi Takahashi, Masatoshi Hagiwara, Tatsuya Sawasaki, Genji Iwasaki, Yu Nakamura, Yo-ichi Nabeshima, David B. Teplow, Minako Hoshi

    PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA   112 ( 32 )   E4465 - E4474   2015.8

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    Neurodegeneration correlates with Alzheimer's disease (AD) symptoms, but the molecular identities of pathogenic amyloid beta-protein (A beta) oligomers and their targets, leading to neurodegeneration, remain unclear. Amylospheroids (ASPD) are AD patient-derived 10- to 15-nm spherical A beta oligomers that cause selective degeneration of mature neurons. Here, we show that the ASPD target is neuronspecific Na+/K+-ATPase alpha 3 subunit (NAK alpha 3). ASPD-binding to NAK alpha 3 impaired NAK alpha 3-specific activity, activated N-type voltage-gated calcium channels, and caused mitochondrial calcium dyshomeostasis, tau abnormalities, and neurodegeneration. NMR and molecular modeling studies suggested that spherical ASPD contain N-terminal-A beta-derived "thorns" responsible for target binding, which are distinct from low molecular-weight oligomers and dodecamers. The fourth extracellular loop (Ex4) region of NAK alpha 3 encompassing Asn(879) and Trp(880) is essential for ASPD-NAK alpha 3 interaction, because tetrapeptides mimicking this Ex4 region bound to the ASPD surface and blocked ASPD neurotoxicity. Our findings open up new possibilities for knowledge-based design of peptidomimetics that inhibit neurodegeneration in AD by blocking aberrant ASPD-NAK alpha 3 interaction.

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  • Effect of sodium pyruvate on exercise intolerance and muscle weakness due to mitochondrial myopathy: A case report Reviewed

    Yasuko Kuroha, Mari Tada, Izumi Kawachi, Masatoyo Nishizawa, Nae Matsubara, Ryoko Koike

    Clinical Neurology   55 ( 6 )   412 - 416   2015

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    We report the case of a 19-year-old woman who had been suffering from general fatigue and exercise intolerance since 15 years old. At 18 years old, she experienced muscle weakness and myalgia of the calves. Six months later, she was admitted to our hospital. She showed muscle weakness of the neck and proximal limbs, and myalgia of the calves was prominent. Serum levels of creatine kinase (CK) and lactic acid were elevated, as was the level of lactic acid in cerebrospinal fluid. T2-weighted and short-inversion-time inversion recovery (STIR) imaging of the lower limbs showed hyperintensity on bilateral gastrocnemius muscles, and the region revealed Gd enhancement. Based on histopathological findings from muscle and identification of a m.3271T&gt
    C point mutation, mitochondrial myopathy was diagnosed. Rest and administration of vitamins B1, and B2, coenzyme Q10, and L-carnitine improved serum CK levels
    however, exercise intolerance, myalgia, and lactic acidemia remained. Sodium pyruvate was then administered, and lactic acid levels, exercise intolerance, and findings on magnetic resonance imaging improved. Sodium pyruvate could prove effective in addressing both elevated serum lactic acid levels and exercise intolerance in mitochondrial disease.

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  • C9ORF72 repeat-associated non-ATG-translated polypeptides are distributed independently of TDP-43 in a Japanese patient with c9ALS Reviewed

    T. Konno, M. Tada, A. Shiga, A. Tsujino, H. Eguchi, M. Masuda-Suzukake, M. Hasegawa, M. Nishizawa, O. Onodera, A. Kakita, H. Takahashi

    NEUROPATHOLOGY AND APPLIED NEUROBIOLOGY   40 ( 6 )   783 - 788   2014.10

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  • Progressive myoclonus epilepsy: extraneuronal brown pigment deposition and system neurodegeneration in the brains of Japanese patients with novel SCARB2 mutations Reviewed

    Y. -J. Fu, I. Aida, M. Tada, M. Tada, Y. Toyoshima, S. Takeda, T. Nakajima, H. Naito, M. Nishizawa, O. Onodera, A. Kakita, H. Takahashi

    NEUROPATHOLOGY AND APPLIED NEUROBIOLOGY   40 ( 5 )   551 - 563   2014.8

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    Aims: Mutations in the SCARB2 gene cause a rare autosomal recessive disease, progressive myoclonus epilepsy (PME) with or without renal failure, the former also being designated action myoclonus-renal failure syndrome. Although reported cases have been accumulating, only a few have described its neuropathology. We studied two Japanese patients with PME without renal failure, in whom the ages at onset and disease durations were 45 and 20 years, and 14 and 8.5 years respectively. Methods: Sequencing and restriction analysis of the SCARB2 gene and neuropathological examination with immunohistochemistry were performed. Results: Gene analyses revealed novel homozygous frameshift and nonsense mutations in the SCARB2 gene. Both cases exhibited deposition of brown pigment in the brain, especially the cerebellar and cerebral cortices. Ultrastructurally, the pigment granules were localized in astrocytes. Neuronal loss and gliosis were also evident in the brain, including the pallidoluysian and cerebello-olivary systems. The spinal cord was also affected. Such changes were less severe in one patient with late-onset disease than in the other patient with early-onset disease. In brain and kidney sections, immunostaining with an antibody against the C-terminus of human SCARB2 revealed decreased levels and no expression of the protein respectively. Conclusions: The frameshift mutation detected in the patient with late-onset disease is a hitherto undescribed, unique type of SCARB2 gene mutation. The present two patients are the first reported to have clearly demonstrated both extraneuronal brown pigment deposition and system neurodegeneration as neuropathological features of PME with SCARB2 mutations.

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  • Pathology and sensitivity of current clinical criteria in corticobasal syndrome Reviewed

    Haruka Ouchi, Yasuko Toyoshima, Mari Tada, Mutsuo Oyake, Izumi Aida, Itsuro Tomita, Akira Satoh, Mitsuhiro Tsujihata, Hitoshi Takahashi, Masatoyo Nishizawa, Takayoshi Shimohata

    MOVEMENT DISORDERS   29 ( 2 )   238 - 244   2014.2

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    The aim of this study was to investigate corticobasal syndrome with respect to underlying pathologies, the ability of current clinical criteria to detect early stages of disease, and symptoms and signs predicting background pathologies. We retrospectively analyzed the clinicopathological findings from patients with corticobasal syndrome. We also analyzed whether those findings fulfilled the diagnostic criteria for corticobasal degeneration (CBD). Finally, we investigated characteristic clinical features that are specific to each background pathology. Of 10 consecutive autopsied patients who had corticobasal syndrome (mean age +/- standard deviation, 67.9 +/- 9.3 years; male:female ratio, 6:4), three had corticobasal degeneration pathology, three had progressive supranuclear palsy, three had Alzheimer's disease, and one had atypical four-repeat tauopathy. Nine patients fulfilled Mayo criteria, and all 10 patients fulfilled modified Cambridge criteria at the later stage, but only two patients fulfilled either clinical criteria within 2 years of disease onset. Five patients fulfilled the clinical criteria for possible CBD (p-CBD), and one patient fulfilled the clinical research criteria for probable sporadic CBD (cr-CBD) at the later stage. Only two patients fulfilled the criteria for either p-CBD or cr-CBD within 2 years of disease onset. Although we could not find any predictive characteristic clinical features that were specific to CBD pathology, only patients with progressive supranuclear palsy developed apraxia of eyelid opening and cerebellar ataxia. Myoclonus and memory impairment, especially if they appear at an early stage of the disease, may predict Alzheimer's disease pathology. Sensitivity of the available clinical criteria for corticobasal syndrome was poor within 2 years of disease onset. (c) 2013 International Parkinson and Movement Disorder Society

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  • Haploinsufficiency of CSF-1R and clinicopathologic characterization in patients with HDLS Reviewed

    Takuya Konno, Masayoshi Tada, Mari Tada, Akihide Koyama, Hiroaki Nozaki, Yasuo Harigaya, Jin Nishimiya, Akiko Matsunaga, Nobuaki Yoshikura, Kenji Ishihara, Musashi Arakawa, Aiko Isami, Kenichi Okazaki, Hideaki Yokoo, Kyoko Itoh, Makoto Yoneda, Mitsuru Kawamura, Takashi Inuzuka, Hitoshi Takahashi, Masatoyo Nishizawa, Osamu Onodera, Akiyoshi Kakita, Takeshi Ikeuchi

    NEUROLOGY   82 ( 2 )   139 - 148   2014.1

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    Objective:To clarify the genetic, clinicopathologic, and neuroimaging characteristics of patients with hereditary diffuse leukoencephalopathy with spheroids (HDLS) with the colony stimulating factor 1 receptor (CSF-1R) mutation.Methods:We performed molecular genetic analysis of CSF-1R in patients with HDLS. Detailed clinical and neuroimaging findings were retrospectively investigated. Five patients were examined neuropathologically.Results:We found 6 different CSF-1R mutations in 7 index patients from unrelated Japanese families. The CSF-1R mutations included 3 novel mutations and 1 known missense mutation at evolutionarily conserved amino acids, and 1 novel splice-site mutation. We identified a novel frameshift mutation. Reverse transcription PCR analysis revealed that the frameshift mutation causes nonsense-mediated mRNA decay by generating a premature stop codon, suggesting that haploinsufficiency of CSF-1R is sufficient to cause HDLS. Western blot analysis revealed that the expression level of CSF-1R in the brain from the patients was lower than from control subjects. The characteristic MRI findings were the involvement of the white matter and thinning of the corpus callosum with signal alteration, and sequential analysis revealed that the white matter lesions and cerebral atrophy relentlessly progressed with disease duration. Spotty calcifications in the white matter were frequently observed by CT. Neuropathologic analysis revealed that microglia in the brains of the patients demonstrated distinct morphology and distribution.Conclusions:These findings suggest that patients with HDLS, irrespective of mutation type in CSF-1R, show characteristic clinical and neuroimaging features, and that perturbation of CSF-1R signaling by haploinsufficiency may play a role in microglial dysfunction leading to the pathogenesis of HDLS.

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  • Hereditary Diffuse Leukoencephalopathy with Spheroids (HDLS): A review of the literature on its clinical characteristics and mutations in the colony-stimulating factor-1 receptor gene

    Takuya Konno, Masayoshi Tada, Mari Tada, Masatoyo Nishizawa, Takeshi Ikeuchi

    Brain and Nerve   66 ( 5 )   581 - 590   2014

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    Hereditary diffuse leukoencephalopathy with spheroids (HDLS) is an early-onset dementia that predominantly affects the cerebral white matter. After the discovery of a gene encoding the colony stimulating factor 1 receptor (CSF-1R) as a causative gene in patients with HDLS, gene analysis of CSF-1R enabled the diagnosis of HDLS without histopathological evidence. To clarify the genetic and clinical characteristics of HDLS, here, we reviewed the characteristics of patients with HDLS with CSF-1R mutations in the literature. Seventy-three patients from 54 pedigrees with HDLS from various ethnic backgrounds have been reported. Among them, Japanese patients account for 22% (16 patients from 15 pedigrees). Mean age at onset was 45 years (18 to 78 years). A wide range of clinical features including cognitive decline, behavioral changes, seizures, pyramidal signs, and parkinsonism have been described in these patients. Various kinds of mutations were found in the tyrosine kinase domain of CSF-1R. A frameshift mutation causing nonsense-mediated mRNA decay was also described. This suggests that haploinsufficiency of CSF-1R is sufficient to cause HDLS. Neuropathological analysis revealed that microglia in the brains of patients demonstrated distinct morphology and distribution. These results suggest that primary microglial dysfunction due to CSF-1R signaling perturbation may underlie the pathogenesis of HDLS.

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  • Relocation of p25 alpha/tubulin polymerization promoting protein from the nucleus to the perinuclear cytoplasm in the oligodendroglia of sporadic and COQ2 mutant multiple system atrophy Reviewed

    Kiyobumi Ota, Masato Obayashi, Kokoro Ozaki, Shizuko Ichinose, Akiyoshi Kakita, Mari Tada, Hitoshi Takahashi, Noboru Ando, Yoshinobu Eishi, Hidehiro Mizusawa, Kinya Ishikawa

    ACTA NEUROPATHOLOGICA COMMUNICATIONS   2   136   2014

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    p25 alpha/tubulin polymerization promoting protein (TPPP) is an oligodendroglial protein that plays crucial roles including myelination, and the stabilization of microtubules. In multiple system atrophy (MSA), TPPP is suggested to relocate from the myelin sheath to the oligodendroglial cell body, before the formation of glial cytoplasmic inclusions (GCIs), the pathologic hallmark of MSA. However, much is left unknown about the re- distribution of TPPP in MSA. We generated new antibodies against the N- and C-terminus of TPPP, and analyzed control and MSA brains, including the brain of a familial MSA patient carrying homozygous mutations in the coenzyme Q2 gene (COQ2). In control brain tissues, TPPP was localized not only in the cytoplasmic component of the oligodendroglia including perinuclear cytoplasm and peripheral processes in the white matter, but also in the nucleus of a fraction (62.4%) of oligodendroglial cells. Immunoelectron microscopic analysis showed TPPP in the nucleus and mitochondrial membrane of normal oligodendroglia, while western blot also supported its nuclear and mitochondrial existence. In MSA, the prevalence of nuclear TPPP was 48.6% in the oligodendroglia lacking GCIs, whereas it was further decreased to 19.6% in the oligodendroglia with phosphorylated a-synuclein (p alpha-syn)-positive GCIs, both showing a significant decrease compared to controls (62.4%). In contrast, TPPP accumulated in the perinuclear cytoplasm where mitochondrial membrane (TOM20 and cytochrome C) and fission (DRP1) proteins were often immunoreactive. We conclude that in MSA-oligodendroglia, TPPP is reduced, not only in the peripheral cytoplasm, but also in the nucleus and relocated to the perinuclear cytoplasm.

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  • Early clinical features of patients with progressive supranuclear palsy with predominant cerebellar ataxia Reviewed

    Masato Kanazawa, Mari Tada, Osamu Onodera, Hitoshi Takahashi, Masatoyo Nishizawa, Takayoshi Shimohata

    PARKINSONISM & RELATED DISORDERS   19 ( 12 )   1149 - 1151   2013.12

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    Background: Patients who develop progressive supranuclear palsy with predominant cerebellar ataxia (PSP-C) develop cerebellar ataxia as the initial and principal symptom, may be misdiagnosed as having multiple system atrophy with predominant cerebellar features (MSA-C). Therefore, we investigated the clinical signs and symptoms between PSP-C and MSA-C early in their disease course.
    Methods: We reviewed the medical records of 15 consecutive patients with pathologically proven PSP-C (4) and MSA-C (11). We recorded the presence or absence of clinical features that developed within 2 years of disease onset.
    Results: The age at onset of PSP-C patients was older than that of MSA-C patients (p = 0.009). The frequencies of falls were higher in PSP-C patients than in MSA-C patients (p = 0.026). Additionally, the development of supranuclear vertical gaze palsy was higher in PSP-C patients than in MSA-C patients (p = 0.011), whereas the frequency of dysautonomia was lower in PSP-C patients than in MSA-C patients (p = 0.035).
    Conclusions: Older onset, early falls, and supranuclear vertical gaze palsy without dysautonomia may predict the diagnosis of PSP-C in patients with late-onset sporadic cerebellar ataxia. (C) 2013 Elsevier Ltd. All rights reserved.

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  • Transportin 1 accumulates in FUS inclusions in adult-onset ALS without FUS mutation. Reviewed

    Takeuchi R, Toyoshima Y, Tada M, Shiga A, Tanaka H, Shimohata M, Kimura K, Morita T, Kakita A, Nishizawa M, Takahashi H

    Neuropathology and applied neurobiology   39 ( 5 )   580 - 584   2013.8

  • Hereditary Diffuse Leukoencephalopathy with Spheroids (HDLS): Clinical Characteristics and Molecular Analyses of CSF-1R Reviewed

    Konno Takuya, Tada Masayoshi, Koyama Akihide, Tada Mari, Sugai Akihiro, Nozaki Hiroaki, Matsunaga Akiko, Harigaya Yasuo, Nishimiya Jin, Ishihara Kenji, Yoneda Makoto, Kakita Akiyoshi, Takahashi Hitoshi, Kawamura Mitsuru, Onodera Osamu, Nishizawa Masatoyo, Ikeuchi Takeshi

    NEUROLOGY   80   2013.2

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  • Early Clinical Features in Japanese Patients with Pathologically Proven Progressive Supranuclear Palsy with Cerebellar Ataxia Reviewed

    Masato Kanazawa, Takayoshi Shimohata, Mari Tada, Osamu Onodera, Hitoshi Takahashi, Masatoyo Nishizawa

    NEUROLOGY   80   2013.2

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  • A fatal neuromuscular disease in an adult patient after poliomyelitis in early childhood: Consideration of the pathology of post-polio syndrome Reviewed

    Takayuki Kosaka, Yasuko Kuroha, Mari Tada, Arika Hasegawa, Takashi Tani, Nae Matsubara, Ryoko Koike, Yasuko Toyoshima, Hitoshi Takahashi

    Neuropathology   33 ( 1 )   93 - 101   2013.2

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    Post-polio syndrome (PPS) characterized by new neuromuscular problems can appear many years after acute poliomyelitis in polio survivors. We report a 77-year-old man with antecedent poliomyelitis who newly developed neuromuscular disease with a clinical course of 27 years, the final 10 years of which were characterized by apparent progression, thus raising doubt as to the clinical diagnosis of amyotrophic lateral sclerosis (ALS) following PPS. Pathologically, plaque-like, old poliomyelitis lesions were found almost exclusively in the lumbosacral cord, showing complete neuronal loss and glial scars in the anterior horns. Although less severe, neuronal loss and gliosis were also evident outside the old lesions, including the intermediate zone. Moreover, symmetrical degeneration of the corticospinal tracts, as evidenced by CD68 immunostaining, was a feature of the white matter of the lower spinal cord. In the motor cortex, loss of Betz cells was also confirmed. Synaptophysin immunostaining of the lumbosacral cord also revealed decreased expression outside the old lesions, excluding the posterior horn. Interestingly, decreased expression of synaptophysin was also evident in the cervical anterior horns, where no old lesions were observed. No Bunina bodies, TDP-43 inclusions, or Golgi fragmentation were found. Neurogenic atrophy was evident in the iliopsoas and scalenus muscles, and inclusion body myositis-like changes were also observed in these muscles and the tongue. Was it possible to have diagnosed this patient as having ALS? We consider that the features in this case may have represented the pathology of long-standing and/or fatal PPS itself, and not ALS. © 2012 Japanese Society of Neuropathology.

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  • Coexistence of Huntington's disease and amyotrophic lateral sclerosis: a clinicopathologic study Reviewed

    Mari Tada, Elizabeth A. Coon, Alexander P. Osmand, Patricia A. Kirby, Wayne Martin, Marguerite Wieler, Atsushi Shiga, Hiroe Shirasaki, Masayoshi Tada, Takao Makifuchi, Mitsunori Yamada, Akiyoshi Kakita, Masatoyo Nishizawa, Hitoshi Takahashi, Henry L. Paulson

    ACTA NEUROPATHOLOGICA   124 ( 5 )   749 - 760   2012.11

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    We report a retrospective case series of four patients with genetically confirmed Huntington's disease (HD) and sporadic amyotrophic lateral sclerosis (ALS), examining the brain and spinal cord in two cases. Neuropathological assessment included a polyglutamine recruitment method to detect sites of active polyglutamine aggregation, and biochemical and immunohistochemical assessment of TDP-43 pathology. The clinical sequence of HD and ALS varied, with the onset of ALS occurring after the mid-50's in all cases. Neuropathologic features of HD and ALS coexisted in both cases examined pathologically: neuronal loss and gliosis in the neostriatum and upper and lower motor neurons, with Bunina bodies and ubiquitin-immunoreactive skein-like inclusions in remaining lower motor neurons. One case showed relatively early HD pathology while the other was advanced. Expanded polyglutamine-immunoreactive inclusions and TDP-43-immunoreactive inclusions were widespread in many regions of the CNS, including the motor cortex and spinal anterior horn. Although these two different proteinaceous inclusions coexisted in a small number of neurons, the two proteins did not co-localize within inclusions. The regional distribution of TDP-43-immunoreactive inclusions in the cerebral cortex partly overlapped with that of expanded polyglutamine-immunoreactive inclusions. In the one case examined by TDP-43 immunoblotting, similar TDP-43 isoforms were observed as in ALS. Our findings suggest the possibility that a rare subset of older HD patients is prone to develop features of ALS with an atypical TDP-43 distribution that resembles that of aggregated mutant huntingtin. Age-dependent neuronal dysfunction induced by mutant polyglutamine protein expression may contribute to later-life development of TDP-43 associated motor neuron disease in a small subset of patients with HD.

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  • Difference in MSA Phenotype Distribution Between Populations: Genetics or Environment? Reviewed

    Tetsutaro Ozawa, Tamas Revesz, Dominic Paviour, Andrew J. Lees, Niall Quinn, Mari Tada, Akiyoshi Kakita, Osamu Onodera, Koichi Wakabayashi, Hitoshi Takahashi, Masatoyo Nishizawa, Janice L. Holton

    JOURNAL OF PARKINSONS DISEASE   2 ( 1 )   7 - 18   2012

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    The reasons for the differences in emphasis on striatonigral or olivopontocerebellar involvement in multiple system atrophy (MSA) remain to be determined. Semi-quantitative pathological analyses carried out in the United Kingdom and Japan demonstrated that olivopontocerebellar-predominant pathology was more frequent in Japanese MSA than British MSA. This observation provides evidence for a difference in phenotype distribution between British and Japanese patients with definite MSA. Studies of the natural history and epidemiology of MSA carried out in various populations have revealed that the relative prevalences of clinical subtypes of MSA probably differ among populations; the majority of MSA patients diagnosed in Europe have predominant parkinsonism (MSA-P), while the majority of MSA patients diagnosed in Asia have predominant cerebellar ataxia (MSA-C). Although potential drawbacks to the published frequencies of clinical subtypes and pathological subtypes should be considered because of selection biases, the difference demonstrated in pathological subtype is also consistent with the differences in clinical subtype of MSA demonstrated between Europe and Asia. Modest alterations in susceptibility factors may contribute to the difference in MSA phenotype distribution between populations. Synergistic interactions between genetic risk variants and environmental toxins responsible for parkinsonism or cerebellar dysfunction should therefore be explored. Further investigations are needed to determine the environmental, genetic, and epigenetic factors that account for the differences in clinicopathological phenotype of MSA among different populations.

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  • The phenotype spectrum of Japanese multiple system atrophy. Reviewed

    Ozawa T, Tada M, Kakita A, Onodera O, Tada M, Ishihara T, Morita T, Shimohata T, Wakabayashi K, Takahashi H, Nishizawa M

    Journal of neurology, neurosurgery, and psychiatry   81 ( 11 )   1253 - 1255   2010.11

  • Isolation and Characterization of Patient-derived, Toxic, High Mass Amyloid beta-Protein (A beta) Assembly from Alzheimer Disease Brains Reviewed

    Akihiko Noguchi, Satoko Matsumura, Mari Dezawa, Mari Tada, Masako Yanazawa, Akane Ito, Manami Akioka, Satoru Kikuchi, Michio Sato, Shouji Ideno, Munehiro Noda, Atsushi Fukunari, Shin-ichi Muramatsu, Yutaka Itokazu, Kazuki Sato, Hitoshi Takahashi, David B. Teplow, Yo-ichi Nabeshima, Akiyoshi Kakita, Kazutomo Imahori, Minako Hoshi

    JOURNAL OF BIOLOGICAL CHEMISTRY   284 ( 47 )   32895 - 32905   2009.11

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    Amyloid beta-protein (A beta) assemblies are thought to play primary roles in Alzheimer disease (AD). They are considered to acquire surface tertiary structures, not present in physiologic monomers, that are responsible for exerting toxicity, probably through abnormal interactions with their target(s). Therefore, A beta assemblies having distinct surface tertiary structures should cause neurotoxicity through distinct mechanisms. Aiming to clarify the molecular basis of neuronal loss, which is a central phenotype in neurodegenerative diseases such as AD, we report here the selective immunoisolation of neurotoxic 10-15-nm spherical A beta assemblies termed native amylospheroids (native ASPDs) from AD and dementia with Lewy bodies brains, using ASPD tertiary structure-dependent antibodies. In AD patients, the amount of native ASPDs was correlated with the pathologic severity of disease. Native ASPDs are anti-pan oligomer A11 antibody-negative, high mass (&gt; 100 kDa) assemblies that induce degeneration particularly of mature neurons, including those of human origin, in vitro. Importantly, their immuno-specificity strongly suggests that native ASPDs have a distinct surface tertiary structure from other reported assemblies such as dimers, A beta-derived diffusible ligands, and A11-positive assemblies. Only ASPD tertiary structure-dependent antibodies could block ASPD-induced neurodegeneration. ASPDs bind presynaptic target(s) on mature neurons and have a mode of toxicity different from those of other assemblies, which have been reported to exert their toxicity through binding postsynaptic targets and probably perturbing glutamatergic synaptic transmission. Thus, our findings indicate that native ASPDs with a distinct toxic surface induce neuronal loss through a different mechanism from other A beta assemblies.

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  • Depletion of medullary serotonergic neurons in patients with multiple system atrophy who succumbed to sudden death Reviewed

    Mari Tada, Akiyoshi Kakita, Yasuko Toyoshima, Osamu Onodera, Tetsutaro Ozawa, Takashi Morita, Masatoyo Nishizawa, Hitoshi Takahashi

    BRAIN   132 ( Pt 7 )   1810 - 1819   2009.7

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    Multiple system atrophy (MSA) is a neurodegenerative disorder characterized by prominent autonomic failure with ataxia and/or parkinsonism. The leading cause of death in MSA is sudden death. We have shown that the early development of autonomic failure is an independent risk factor for sudden death. The depletion of sympathetic preganglionic neurons in the spinal intermediolateral cell column (IML) and its afferent medullary catecholaminergic and serotonergic neurons has been proposed to be partly responsible for autonomic failure in MSA. In this study, we investigated whether the depletion of neurons in any of these autonomic neuron groups contributes to sudden death in MSA. Out of 52 autopsy-proven patients with MSA, we selected 12 individuals who had died within 3.5 years after disease onset to define the accurate levels of slices and identify early neuropathological changes of autonomic nuclei in MSA. Four patients succumbed to sudden death and eight patients died through established causes. Serial 10 mu m sections were obtained from the 8th segment of the thoracic cord and the rostral medulla oblongata. Sections from the medulla oblongata were immunostained for thyrosine hydroxylase and tryptophan hydroxylase. The total cell number in the five sections was computed for comparison. Compared with the control, the MSA group showed a marked depletion of neurons in the IML (38.0 +/- 7.1 versus 75.2 +/- 7.6 cells, P &lt; 0.001), thyrosine hydroxylase-immunoreactive neurons in the ventrolateral medulla (VLM) (17.4 +/- 5.1 versus 72.8 +/- 13.6 cells, P &lt; 0.01) and tryptophan hydroxylase-immunoreactive neurons in the VLM (15.6 +/- 9.2 versus 60.8 +/- 17.0 cells, P &lt; 0.01), nucleus raphe obscurus (19.3 +/- 4.4 versus 75.3 +/- 8.6 cells, P &lt; 0.001), nucleus raphe pallidus (2.1 +/- 2.7 versus 9.0 +/- 3.4 cells, P &lt; 0.03), and arcuate nucleus (0.4 +/- 0.8 versus 2.3 +/- 1.5 cells, P &lt; 0.05). Moreover, in patients who succumbed to sudden death, when compared with patients who had established causes of death, we found a marked depletion of tryptophan hydroxylase-immunoreactive neurons in the VLM (7.3 +/- 3.5 versus 21.8 +/- 6.5 cells, P &lt; 0.02) and nucleus raphe obscurus (15.0 +/- 2.0 versus 22.5 +/- 2.1 cells, P &lt; 0.01). The results indicate that the spinal IML and medullary catecholaminergic and serotonergic systems are involved even in the early stages of MSA, and the dysfunction of the medullary serotonergic system regulating cardiovascular and respiratory systems could be responsible for sudden death in patients with MSA.

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  • Cerebellar Involvement in Progressive Supranuclear Palsy: A Clinicopathological Study Reviewed

    Masato Kanazawa, Takayoshi Shimohata, Yasuko Toyoshima, Mari Tada, Akiyoshi Kakita, Takashi Morita, Tetsutaro Ozawa, Hitoshi Takahashi, Masatoyo Nishizawa

    MOVEMENT DISORDERS   24 ( 9 )   1312 - 1318   2009.7

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    The clinical heterogeneity of progressive supranuclear palsy (PSP), which is classified as classic Richardson&apos;s syndrome (RS) and PSP-Parkinsonism (PSP-P), has been previously discussed. We retrospectively analyzed 22 consecutive Japanese patients with pathologically proven PSP to investigate the clinicopathological heterogeneity. We investigated the clinical features both early in and at any time during the disease course. The pathological severities of neuronal loss with gliosis and tau pathology were also evaluated. On the basis of the clinical features, 10 patients were categorized as having RS, and 8 were categorized as having PSP-P. Four patients presenting with cerebellar ataxia or cerebral cortical signs were categorized as having unclassifiable PSP. Among them, 3 developed cerebellar ataxia as the initial and principal symptom. Notably, tau-positive inclusion bodies in Purkinje cells were significantly more frequently observed in the patients with cerebellar ataxia than in those without cerebellar ataxia. All the patients with cerebellar ataxia exhibited more neuronal loss with gliosis and higher densities of coiled bodies in the cerebellar dentate nucleus than those without cerebellar ataxia. This study confirms the wide spectrum of clinicopathological manifestations associated with PSP regardless of different ethnic origin, and demonstrates that PSP patients manifest cerebellar ataxia. (C) 2009 Movement Disorder Society

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  • Marinesco-Sjogren syndrome with atrophy of the brain stem tegmentum and dysplastic cytoarchitecture in the cerebral cortex Reviewed

    Kenji Sakai, Mari Tada, Yosuke Yonemochi, Takashi Nakajima, Osamu Onodera, Hitoshi Takahashi, Akiyoshi Kakita

    NEUROPATHOLOGY   28 ( 5 )   541 - 546   2008.10

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    Marinesco-Sjogren syndrome (MSS) is a progressive multisystem disease with autosomal recessive inheritance characterized by cataracts, mental retardation, and cerebellar ataxia. Recently, two causative genes for MSS, SIL1 and SARA2, have been identified. On the other hand, the histopathologic features of the CNS in this syndrome have not yet been clarified in detail. We report here the features of an autopsy case of MSS with progressive myopathy, in which atrophy of the cerebellum and brain stem tegmentum, retinal degeneration, and dysplastic cytoarchitecture in the cerebral cortex were evident. An elder brother of the patient showed quite similar symptoms, implying an autosomal recessive mode of inheritance. However, we detected no mutations in the available genes. This case appears to represent an unusual example of MSS manifesting widespread developmental anomaly and neuronal degeneration in the CNS.

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  • The wide spectrum of clinicopathological manifestations in pathologically proven progressive supranuclear palsy: A study of Japanese patients Reviewed

    Kanazawa Masato, Shimohata Takayoshi, Toyoshima Yasuko, Tada Mari, Kakita Akiyoshi, Ozawa Tetsutaro, Morita Takashi, Takahashi Hitoshi, Nishizawa Masatoya

    NEUROLOGY   70 ( 11 )   A385   2008.3

  • Distinct clinical phenotypes of pathologically proven progressive supranuclear palsy: Richardson's syndrome, PSP-Parkinsonism and PSP-cerebral cortical dysfunction Reviewed

    Masato Kanazawa, Takayoshi Shimohata, Akiyoshi Kakita, Mari Tada, Yasuko Toyoshima, Takashi Morita, Hitoshi Takahashi, Masatoyo Nishizawa

    NEUROLOGY   68 ( 12 )   A49 - A49   2007.3

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  • Early development of autonomic dysfunction may predict poor prognosis in patients with multiple system atrophy Reviewed

    Mari Tada, Osamu Onodera, Masayoshi Tada, Tetsutaro Ozawa, Yue-Shan Piao, Akiyoshi Kakita, Hitoshi Takahashi, Masatoyo Nishizawa

    ARCHIVES OF NEUROLOGY   64 ( 2 )   256 - 260   2007.2

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    Background: Multiple system atrophy (MSA) is diverse in clinical phenotype, disease progression, and prognosis. Sudden death is a leading cause of death in patients with MSA.
    Objective: To determine what clinical factors affect the progression and survival prognosis of those with MSA.
    Design: A retrospective review of the medical records of 49 consecutive Japanese patients with pathologically confirmed MSA ( 29 men and 20 women; mean +/- SD age at onset, 59.8 +/- 6.5 years). Cox proportional hazards models were used to compare the risks of being in a wheel-chair-bound state, being in a bedridden state, and having a shorter survival.
    Results: Thirty-one patients were diagnosed as having cerebellar type MSA, and 18 were diagnosed as having parkinsonian type MSA. Twenty-nine patients with cerebellar type MSA and 17 patients with parkinsonian type MSA had autonomic dysfunction. The median times from disease onset to being in a wheel-chair-bound state, being in a bedridden state, death, and the development of autonomic dysfunction were 3.5, 5.0, 7.0, and 2.5 years, respectively. Patients with an early development of autonomic dysfunction (within 2.5 years from the onset of MSA) had significantly higher risks of being in a wheel-chair-bound state (multivariate-adjusted hazard ratio [HR], 4.32; 95% confidence interval [CI], 2.04-9.15), being in a bedridden state (HR, 3.87; 95% CI, 1.77-8.48), having a shorter survival (HR, 3.40; 95% CI, 1.61-7.15), and sudden death (HR, 7.22; 95% CI, 1.49-35.07).
    Conclusion: The early development of autonomic dysfunction is an independent predictive factor for rapid disease progression and shorter survival in patients with MSA.

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  • Long-terms therapeutic efficacy and safety of low-dose tacrolimus (FK506) for myasthenia gravis Reviewed

    Masayoshi Tada, Takayoshi Shimohata, Mari Tada, Mutsuo Oyake, Shuichi Igarashi, Osamu Onodera, Satoshi Naruse, Keiko Tanaka, Shoji Tsuji, Masatoyo Nishizawa

    JOURNAL OF THE NEUROLOGICAL SCIENCES   247 ( 1 )   17 - 20   2006.8

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    Objective: To elucidate the long-term therapeutic efficacy and safety of low-dose FK506 (tacrolimus) in patients with myasthenia gravis (MG).
    Patients and methods: We treated nine patients with MG (all women: age range: 35-83years (mean: 51.1 years); MGFA classification: 4 type IIa, 4 type IIb, and 1 type IVb patients) with FK506 for more than 24months (observation period: 24-46months). All the patients had undergone extended thymectomy before FK506 treatment; two patients (22.2%) had noninvasive thymoma and six (66.7%) had thymic hyperplasia. We evaluated total Quantitative MG (Q-MG) score, anti-acetylcholine receptor (AM) antibody titer in the blood, interleukin 2 (IL-2) production in peripheral blood mononuclear cells (PBMCs), administration dosage of prednisolone (PSL), and adverse effects of FK506.
    Results: A reduction in steroid dosage of 50 50% without worsening of the symptoms was observed 1 year after FK506 administration in three out of six steroid-dependent MG patients (50.0%). The total Q-MG scores (range: 0-39 points) at 6months and l year after FK506 administration improved by 3 points or more in six (66.7%) and seven (77.8 %) out of nine patients, respectively. The efficacy of FK506 was maintained for more than 2years. Although adverse effects were observed in three patients (33.3 %), these were not serious.
    Conclusions: Our study indicates that low-dose FK506 treatment may be efficacious not only in controlling intractable myasthenic symptoms, but also in reducing steroid dosage, and that FK506 is safe as an adjunctive drug to PSL for MG treatment for a maximum of 3 years. (c) 2006 Elsevier B.V. All rights reserved.

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  • Multiple gas-forming brain microabscesses due to Klebsiella pneumoniae Reviewed

    M Tada, Y Toyoshima, H Honda, N Kojima, T Yamamoto, K Nishikura, H Takahashi

    ARCHIVES OF NEUROLOGY   63 ( 4 )   608 - 609   2006.4

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  • 切迫脳ヘルニアをきたした非ヘルペス性急性髄膜脳炎に対する低体温療法の試み

    寺島 健史, 富樫 優, 他田 真理, 本多 忠幸, 西澤 正豊

    神経治療学   22 ( 4 )   513 - 517   2005.7

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  • Babinski-Nageotte syndrome with ipsilateral hemiparesis Reviewed

    M Tada, M Tada, H Ishiguro, K Hirota

    ARCHIVES OF NEUROLOGY   62 ( 4 )   676 - 677   2005.4

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  • An autopsy case of systemic vasculitis associated with hepatitis C virus-related mixedcryoglobulinemia presenting severe peripheral neuropathy Reviewed

    Mari Tada, Satoshi Naruse, Aki Arai, Aki Sato, Keiko Tanaka, Yue-Shan Piao, Akiyoshi Kakita, Hitoshi Takahashi, Masatoyo Nishizawa, Shoji Tsuji

    Clinical Neurology   44 ( 10 )   686 - 690   2004.10

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    A 75-year-old man, previously diagnosed as having chronic hepatitis C virus (HCV) infection, suddenly developed left foot drop, followed by progressive motor weakness and sensory disturbance in all of the extremities. Because of an elevated level of the rheumatoid factor (RF), he had been treated with antirheumatic drugs three years before the onset of his neurological symptoms. Within two months, he became unable to walk any more, and was transferred to our hospital. Neurologic examination showed asymmetrical severe muscular weakness and atrophy of all the limbs, and a sensory deficit under the level of the wrists and knees. Livedo reticularis was also noted in bilateral legs. Nerve conduction study revealed severe sensorimotor axonal neuropathy, and muscle biopsy specimens showed necrotizing vasculitis of small arteries in the perimysium, Serological tests indicated type II cryoglobulinemia (monoclonal IgAκ + polyclonal IgG). A diagnosis of vasculitic neuropathy associated with HCV-related mixed cryoglobulinemia was made. A high-dose intravenous immunoglobulin therapy (IVIg) and a high-dose steroid therapy were not effective, and he died of alveolar hemorrhage probably due to pulmonary vasculitis. Postmortem pathological examination revealed severe vasculitis, accompanied by fibrinoid degeneration and the infiltration of predominant mononuclear cells into the small and medium-sized vascular walls of multiple organs such as the liver, kidney, pancreas and intestine as well as the peripheral nerves and skeletal muscles. A severe loss of myelinated fibers were also observed in the multiple peripheral nerves examined. We emphasize that patients with HCV infection and mixed cryoglobulinemia may develop severe systemic vasculitis resembling polyarteritis nodosa leading to often life-threatening polyvisceral failure, particularly in patients showing progressive mononeuropathy multiplex.

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  • [MRI findings of hypertensive brainstem encephalopathy]. Reviewed

    Tada M, Kashida S, Shindo M, Kojima N

    No to shinkei = Brain and nerve   56 ( 4 )   362 - 363   2004.4

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  • Steroid-pulse therapy in Guillain-Barré syndrome associated with cytomegalovirus infection: A case report Reviewed

    Masayoshi Tada, Osamu Onodera, Izumi Kawachi, Kenju Hara, Masahisa Sato, Hiide Yoshino, Atsuko Asano, Yoshiaki Soma, Shoji Tsuji

    Brain and Nerve   55 ( 7 )   615 - 621   2003.7

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    We report a 27-year-old man with Guillain-Barré syndrome (GBS) preceded by cytomegalovirus infection. He was admitted to our hospital because of distal dominant weakness and sensory disturbance 5 days after fever. Double filtration plasmapheresis (DFPP) was performed and clinical symptoms temporary but dramatically improved. However facial nerve palsy, difficulty in swallowing food, weakness, dysautonomia and respiratory failure rapidly progressed within 5 days áfter the onset. Repeated DFPP failed to improve his symptoms. Two months after the onset, he did not improve at all. On T1-weighted MRI, nerve roots were still enhanced with gadolinium, and CSF examination revealed 1,324 mg/dl of protein. These findings suggested us the existence of continuous inflammation on nerve roots. We gave steroid-pulse therapy. He dramatically improved after this treatment. We repeated steroid-pulse therapy for seven times. He was discharged without any major complication 6 months after the onset. Steroid-pulse therapy should be considered in GBS patients associated with CMV infection when other conventional treatments are ineffective.

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  • Eczematous reactions after intravenous immunoglobulin therapy in two patients with Guillain-Barré syndrome and a patient with Miller Fisher syndrome Reviewed

    Masayoshi Tada, Mari Tada, Hideaki Ishiguro, Eiichi Yagi, Kouichi Hirota

    Brain and Nerve   55 ( 5 )   401 - 405   2003.5

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    The use of intravenous immunoglobulin (IVIG) has become an accepted treatment for patients with Guillain-Barré syndrome. Few patients develop adverse reactions to MG such as flushing, urticaria, eczema, chest tightness, wheezing, diaphoresis and hypotension. We report three patients who each recieved a five day course of MG at the standard dose of 0.4 g/kg/day. Two patients had Guillain-Barré syndrome, and the other had Miller Fisher syndrome. All developed eczematous reactions after 4 days from the start day of therapy to 5 days from the last day of therapy. One patient with GBS had widespread eczematous eruption with severe pompholyx lesions on the palms, fingers and soles, and spread over a period of 2 to 3 weeks to become generalized. That persisted for 4 weeks but gradually settled with desquamation by the use of topical steroids. None of our patients subsequently developed long-term or chronic eczema after the resolution of the initial cutaneous reaction. Eczematous reactions of our patients were similar to those reported in the literature and clinically typical as pompholyx. Although pompholyx has been recognized as a clinical entity, its cause remains obscure. Cutaneous reactions after IVIG infusion are recognized to be rare, but actually they may occur more frequently than our recognition, and its knowledge is essential to make the right clinical decision.

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  • Two cases of lumbosacral radiculopathy after intra-arterial infusion of cisplatin for treatment of uterine cancer Reviewed

    Kenju Hara, Mari Tada, Satoshi Naruse, Yoshiaki Soma, Yumi Kojima, Hitoshi Kurata, Kenichi Tanaka, Shoji Tsuji

    Clinical Neurology   43 ( 1-2 )   26 - 30   2003.1

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    A 60-year-old woman (case 1) experienced severe pain in the lower part of her leg and sciatic nerve paralysis the following day after intra-arterial infusion of cisplatin for the treatment of uterine body cancer. The symptoms gradually improved in the next six months. The lesion was not detected on pelvic MRI after two months. A 49-year-old woman (case 2) complained of severe pain in the lower part of her leg three days after intra-arterial infusion of cisplatin for the treatment of uterocervical cancer. Enhancement of the right first sacral root was demonstrated by the pelvic MRI. The symptoms gradually improved with the symptomatic therapy. To our knowledge, this is the first report of lumbo-sacral radiculopathy associated with intra-arterial infusion of cisplatin presenting the enhanced lesion in the root on MRI. It was suggested that lumbo-sacral radiculopathy induced by intra-arterial infusion of cisplatin is not a rare complication and that MRI is useful in confirming the diagnosis. Various precautions should be undertaken to prevent such complications.

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  • Consciousness disturbance caused by iodoform absorption in a patient with decubitus ulcer topically treated with iodoform-gauze Reviewed

    Masayoshi Tada, Mari Tada, Hideaki Ishiguro, Kouichi Hirota

    Brain and Nerve   54 ( 12 )   1051 - 1054   2002.12

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    A 76-year-old man with supranuclear palsy, developed consciousness disturbance followed by the treatment of decubitus ulcer in the sacral region using iodoform-gauze. He was semicoma and tachycardia. His pupils were miotic and light reflexes were absent. EEG demonstrated diffuse and random slow activities. Plasma concentration of free iodine was high (151 μ g/dl), but the other laboratory findings including thyroid functions were normal. He was diagnosed as suffering from iodoform poisoning. The symptoms and laboratory abnormalities of the patient recovered soon after the removal of iodoform-gauze. Although iodoform has been widely used for the treatment of wounds, there are few case reports of its side effects, such as consciousness disturbance, delirium, headache and tachycardia.

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  • 眼で見る神経内科 Claude症候群のMRI所見 Reviewed

    他田 正義, 他田 真理, 石黒 英明, 廣田 紘一

    神経内科   57 ( 3 )   272 - 274   2002.9

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  • 健常男性にみられたクリプトコッカス髄膜脳炎の1例 日和見感染者でのクリプトコッカス髄膜脳炎との相違点 Reviewed

    他田 真理, 藤田 信也, 永井 博子

    神経内科   56 ( 2 )   179 - 184   2002.2

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  • 長岡赤十字病院における脳血管障害の検討

    藤田 信也, 高橋 俊昭, 長谷川 有香, 他田 真理, 永井 博子, 玉谷 真一, 大石 誠, 吉村 淳一, 関原 芳夫, 本山 浩, 外山 孚

    長岡赤十字病院医学雑誌   14 ( 1 )   21 - 25   2001.9

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    1999〜2000年の2年間に入院した脳血管障害患者2022例について検討した.脳血管障害患者は,神経内科で46.3%,脳外科で35.3%,全体で40.7%を占めた.各病型別の脳血管障害に対する内訳は,脳出血179例,脳梗塞505例,TIA/VBIが58例,SAHが81例であった.脳出血例の病型は,被殻出血が35.8%と最も多く,視床出血32.4%,皮質下出血14.5%,小脳出血10.6%,橋出血6.7%であった.平均入院数は41.7日で,死亡率は15.6%であった.危険因子として,脳出血患者の65.4%に高血圧症がみられた.虚血性脳血管障害563例の病型は,ラクナ梗塞34.5%が最も多く,脳血栓29.0%,脳塞栓26.2%,TIA/VBIが10.3%であった.平均在院日数は脳塞栓が37.0日と最も長く,脳血栓31.9日,ラクナ梗塞21.3日,TIA9.9日,VBI7.7日であった.危険因子として,脳塞栓患者の57.4%で心房細動,ラクナ梗塞の57.7%で高血圧症を認めた

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  • 胃検診を契機に診断されたCowden病の1例 Reviewed

    八木 一芳, 他田 真理, 田口 澄人, 後藤 俊夫, 大原 一彦, 小田 栄司, 櫻井 金三, 関根 厚雄, 阿部 道行, 飯泉 俊雄

    胃と腸   34 ( 8 )   1063 - 1068   1999.7

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    DOI: 10.11477/mf.1403102790

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Books

  • 非定型パーキンソニズム-基礎と臨床-

    下畑享良編、他田真理、柿田明美 他( Role: Contributor ,  II-1. 多系統萎縮症. c 病理.)

    文光堂  2019.5 

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  • 高齢発症多系統萎縮症の臨床病理学的検討

    荻根沢 真也, 今野 卓哉, 清水 宏, 他田 真理, 柿田 明美, 小野寺 理

    パーキンソン病・運動障害疾患コングレスプログラム・抄録集   14回   112 - 112   2021.2

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  • Clinicopathologic study of two patients with amyotrophic lateral sclerosis harboring TBK1 mutations

    TADA Mari, HATANO Yuya, TAKESHIMA Akari, SAITO Rie, SAJI Etsuji, TOKUTAKE Takayoshi, ISHIHARA Tomohiko, TOYOSHIMA Yasuko, ONODERA Osamu, KAKITA Akiyoshi

    日本神経学会学術大会プログラム・抄録集   62nd   2021

  • 神経変性疾患領域の基盤的調査研究 孤発性ALSにおける認知症発症リスクとしてのAPOE2

    小野寺理, 畠野雄也, 石原智彦, 他田真理, 柿田明美

    神経変性疾患領域の基盤的調査研究 令和2年度 総括・分担研究報告書(Web)   2021

  • 本邦の孤発性ALSにおけるAPOE2の認知症への影響の検討

    畠野 雄也, 石原 智彦, 他田 真理, 柿田 明美, 小野寺 理

    Dementia Japan   34 ( 4 )   521 - 521   2020.10

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  • COX10変異とPMP22欠失を伴った白質脳症の一家系 分子遺伝学的解析

    石黒 敬信, 黒羽 泰子, 原 範和, 目崎 直実, 三浦 健, 春日 健作, 長谷川 有香, 谷 卓, 高橋 哲哉, 松原 奈絵, 他田 真理, 河内 泉, 柿田 明美, 小野寺 理, 小池 亮子, 池内 健

    臨床神経学   58 ( Suppl. )   S327 - S327   2018.12

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  • COX10変異とPMP22欠失を伴った白質脳症の一家系 臨床病理学的解析

    黒羽 泰子, 石黒 敬信, 長谷川 有香, 谷 卓, 高橋 哲哉, 松原 奈絵, 他田 真理, 河内 泉, 柿田 明美, 小野寺 理, 池内 健, 小池 亮子

    臨床神経学   58 ( Suppl. )   S327 - S327   2018.12

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  • COX10変異とPMP22欠失を伴った白質脳症の一家系 臨床病理学的解析

    黒羽 泰子, 石黒 敬信, 長谷川 有香, 谷 卓, 高橋 哲哉, 松原 奈絵, 他田 真理, 河内 泉, 柿田 明美, 小野寺 理, 池内 健, 小池 亮子

    臨床神経学   58 ( Suppl. )   S327 - S327   2018.12

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  • ALS診断におけるAwaji基準の有用性に関する、当科剖検例での後方視的検討

    茂木 崇秀, 石原 智彦, 竹島 明, 他田 真理, 他田 正義, 柿田 明美, 小野寺 理

    臨床神経学   58 ( Suppl. )   S265 - S265   2018.12

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  • Neuropathologic Subtypes of Frontotemporal Lobar Degeneration. Invited

    Mari Tada, Akiyoshi Kakita

    BRAIN and NERVE   70 ( 5 )   0501 - 0516   2018.5

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    <文献概要>前頭側頭葉変性症(FTLD)は,多様な背景病理と遺伝子変異を含む不均一な疾患群である。近年,いくつかの関連遺伝子の発見と,脳内に異常蓄積する蛋白の同定により,FTLDの大部分がFTLD-tau,FTLD-TDP,FTLD-FUSに分類されることが明らかになった。本稿では各群の主要な疾患の組織像について述べ,臨床病型および遺伝子変異との関連について概説する。

    DOI: 10.11477/mf.1416201033

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  • 臨床医のための神経病理再入門 ミクログリアの組織学的特徴 Invited

    他田 真理, 柿田 明美

    Clinical Neuroscience   36 ( 3 )   276 - 277   2018.3

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  • リウマチ性多発筋痛症と診断され、ステロイド治療中に症状が増悪して確診に至った血管炎の1生検例

    宮平 鷹揚, 中村 昭則, 武井 洋一, 小口 賢哉, 菅野 祐幸, 大原 慎司, 他田 真理

    信州医学雑誌   66 ( 1 )   109 - 110   2018.2

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  • 長期間精神症状が先行した、PSEN1遺伝子変異を有する早期発症型家族性アルツハイマー病の1剖検例

    竹島 明, 他田 真理, 鈴木 正博, 春日 健作, 池内 健, 小野寺 理, 高橋 均, 柿田 明美, 伊古田 勇人

    信州医学雑誌   66 ( 1 )   110 - 111   2018.2

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  • 長期間精神症状が先行した、PSEN1遺伝子変異を有する早期発症型家族性アルツハイマー病の1剖検例

    竹島 明, 他田 真理, 鈴木 正博, 春日 健作, 池内 健, 小野寺 理, 高橋 均, 柿田 明美, 伊古田 勇人

    信州医学雑誌   66 ( 1 )   110 - 111   2018.2

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  • 常染色体劣性遺伝性が疑われる若年発症 緩徐進行性小脳失調症の1剖検例

    齋藤 理恵, 他田 真理, 若林 允甫, 小野寺 理, 高橋 均, 池内 健, 柿田 明美, 横尾 英明

    信州医学雑誌   66 ( 1 )   111 - 112   2018.2

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  • 認知症を呈する白質脳症 病理から見た病態形成 グリア細胞の関与

    他田 真理, 高橋 均, 柿田 明美

    Dementia Japan   31 ( 4 )   531 - 531   2017.10

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  • 12年前の腎生検組織でエオジン好性核内封入体が認められた神経核内封入体病の1例

    元木 三記子, 吉本 幸世, 宇野田 喜一, 石田 志門, 中嶋 秀人, 木村 文治, 荒若 繁樹, 佐藤 朋江, 他田 真理, 柿田 明美

    臨床神経学   57 ( 10 )   657 - 657   2017.10

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  • 進行性骨化性線維異形成症の1剖検例

    田中 英智, 豊島 靖子, 他田 真理, 清水 宏, 米持 洋介, 小澤 哲夫, 中島 孝, 高橋 均, 柿田 明美

    新潟医学会雑誌   131 ( 5 )   315 - 316   2017.5

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  • 原発性側索硬化症と診断したが、進行性核上性麻痺と病理診断された症例の臨床病理学

    米持 洋介, 飛永 雅信, 池田 哲彦, 遠藤 寿子, 大田 健太郎, 会田 泉, 中島 孝, 高原 誠, 今里 真, 小澤 哲夫, 三吉 政道, 金谷 洋, 横山 裕一, 他田 真理, 柿田 明美, 高橋 均

    臨床神経学   56 ( Suppl. )   S446 - S446   2016.12

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  • HDLS患者脳におけるミクログリアの形態学的異常 Microgliopathyとして

    他田 真理, 高橋 均, 柿田 明美

    臨床神経学   55 ( Suppl. )   S122 - S122   2015.12

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  • 多系統萎縮症におけるアストロサイト特異的タンパク質の解析

    星 明彦, 角田 綾子, 宇川 義一, 西澤 正豊, 他田 真理, 柿田 明美

    脳循環代謝   27 ( 1 )   194 - 194   2015.10

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  • 拘束性換気障害を契機に76歳時に診断された球脊髄性筋萎縮症の1剖検例

    長谷川 有香, 黒羽 泰子, 谷 卓, 松原 奈絵, 他田 真理, 柿田 明美, 小池 亮子

    臨床神経学   55 ( 8 )   608 - 608   2015.8

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  • 末梢神経障害と後索変性を伴った中年期発症の脊髄小脳変性症の1剖検例

    齋藤 理恵, 他田 真理, 谷 卓, 小池 亮子, 五十嵐 修一, 山崎 元義, 小野寺 理, 西澤 正豊, 高橋 均, 柿田 明美

    信州医学雑誌   63 ( 1 )   70 - 71   2015.2

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  • 多系統萎縮症でのtubulin polymerization promoting protein(TPPP)の細胞内局在変化

    太田 浄文, 大林 正人, 尾崎 心, 市野瀬 志津子, 他田 真理, 柿田 明美, 高橋 均, 石川 欽也, 水澤 英洋

    臨床神経学   54 ( Suppl. )   S197 - S197   2014.12

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  • 大脳皮質基底核変性症の臨床診断基準の検討

    下畑 享良, 大内 東香, 豊島 靖子, 他田 真理, 小宅 睦郎, 会田 泉, 冨田 逸郎, 佐藤 聡, 辻畑 光宏, 高橋 均, 西澤 正豊

    臨床神経学   54 ( Suppl. )   S66 - S66   2014.12

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  • SCARB2変異を認めた進行性ミオクローヌスてんかん2剖検例の臨床病理・生化学的解析

    他田 正義, 付 永娟, 会田 泉, 他田 真理, 武田 茂樹, 豊島 靖子, 中島 孝, 内藤 明彦, 高橋 均, 小野寺 理, 西澤 正豊

    臨床神経学   54 ( Suppl. )   S68 - S68   2014.12

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  • HDLSはCSF-1Rの機能喪失で生じる シグナル伝達障害とハプロ不全

    勇 亜衣子, 今野 卓哉, 他田 正義, 他田 真理, 小山 哲秀, 野崎 洋明, 金田 大太, 田代 裕一, 山本 徹, 高橋 均, 西澤 正豊, 小野寺 理, 柿田 明美, 池内 健

    臨床神経学   54 ( Suppl. )   S8 - S8   2014.12

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  • 筋萎縮性側索硬化症のTDP-43大脳皮質組織像の多様性 臨床病理および生化学的解析

    竹内 亮子, 他田 真理, 志賀 篤, 今野 卓哉, 豊島 靖子, 小野寺 理, 西澤 正豊, 柿田 明美, 高橋 均

    臨床神経学   54 ( Suppl. )   S200 - S200   2014.12

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  • 神経軸索スフェロイドを伴う白質脳症HDLS Microgliaの組織学的異常

    他田 真理, 今野 卓哉, 他田 正義, 岡崎 健一, 荒川 武蔵, 伊東 恭子, 山本 徹, 横尾 英明, 吉倉 延亮, 石原 健司, 豊島 靖子, 小野寺 理, 西澤 正豊, 池内 健, 高橋 均, 柿田 明美

    臨床神経学   54 ( Suppl. )   S214 - S214   2014.12

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  • 神経変性疾患におけるアクアポリンと内向き整流性カリウムチャネル4.1の解析

    星 明彦, 角田 綾子, 宇川 義一, 西澤 正豊, 他田 真理, 柿田 明美, 高橋 均

    臨床神経学   54 ( Suppl. )   S135 - S135   2014.12

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  • Astrocyteにおけるタウの蓄積像に着目したPSP関連タウオパチーの連続性について

    横山 裕一, 豊島 靖子, 他田 真理, 志賀 篤, 池内 健, 長谷川 一子, 染矢 俊幸, 柿田 明美, 高橋 均

    Dementia Japan   28 ( 4 )   508 - 508   2014.10

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  • Background pathologies and sensitivity of the current clinical criteria in corticobasal syndrome

    T. Shimohata, H. Ouchi, Y. Toyoshima, M. Tada, H. Takahashi, M. Nishizawa

    MOVEMENT DISORDERS   29   S128 - S128   2014.5

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  • 神経変性疾患に関する調査研究 筋萎縮性側索硬化症の大脳皮質におけるTDP-43組織像の多様性の検討:臨床病理,および生化学的解析

    高橋均, 竹内亮子, 竹内亮子, 他田真理, 志賀篤, 今野卓哉, 豊島靖子, 小野寺理, 西澤正豊, 柿田明美

    神経変性疾患に関する調査研究 平成25年度 総括・分担研究報告書   2014

  • 異常タンパク伝播仮説に基づく神経疾患の画期的治療法の開発 C9ORF72変異を有する日本人ALSの一剖検例

    高橋均, 今野卓哉, 他田真理, 志賀篤, 西澤正豊, 小野寺理, 柿田明美

    異常タンパク伝播仮説に基づく神経疾患の画期的治療法の開発 平成25年度 総括・分担研究報告書   2014

  • 運動失調症の病態解明と治療法開発に関する研究 多系統萎縮症におけるtubulin polymerization promoting protein(TPPP/p25α)の細胞内局在変化

    水澤英洋, 石川欽也, 太田浄文, 尾崎心, 他田真理, 柿田明美, 高橋均

    運動失調症の病態解明と治療法開発に関する研究 平成25年度 総括・分担研究報告書   2014

  • 小脳性運動失調を伴う進行性核上性麻痺の病初期臨床像の検討

    金澤 雅人, 下畑 享良, 他田 真理, 小野寺 理, 高橋 均, 西澤 正豊

    臨床神経学   53 ( 12 )   1467 - 1467   2013.12

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  • パーキンソン病大脳皮質におけるアクアポリン発現とα-synuclein病理の検討

    星 明彦, 角田 綾子, 宇川 義一, 西澤 正豊, 他田 真理, 柿田 明美, 高橋 均

    臨床神経学   53 ( 12 )   1590 - 1590   2013.12

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  • Corticobasal syndromeの臨床診断基準の感度および臨床症候の検討

    下畑 享良, 大内 東香, 豊島 靖子, 他田 真理, 小宅 睦郎, 會田 泉, 冨田 逸郎, 辻畑 光宏, 佐藤 聡, 高橋 均, 西澤 正豊

    臨床神経学   53 ( 12 )   1613 - 1613   2013.12

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  • 神経軸索スフェロイドを伴う白質脳症HDLSにおけるCSF1Rシグナル伝達異常の解析

    今野 卓哉, 他田 正義, 小山 哲秀, 他田 真理, 荒川 武蔵, 野崎 洋明, 針谷 康夫, 西宮 仁, 松永 晶子, 米田 誠, 吉倉 延亮, 犬塚 貴, 石原 健司, 河村 満, 高橋 均, 小野寺 理, 西澤 正豊, 池内 健

    臨床神経学   53 ( 12 )   1529 - 1529   2013.12

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  • 筋萎縮性側索硬化症の大脳皮質におけるTDP-43の組織学的および生化学的解析

    竹内 亮子, 志賀 篤, 他田 真理, 今野 卓哉, 豊島 靖子, 柿田 明美, 小野寺 理, 西澤 正豊, 高橋 均

    臨床神経学   53 ( 12 )   1535 - 1535   2013.12

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  • 神経軸索スフェロイドを伴う白質脳症HDLS Microgliaの組織学的解析

    他田 真理, 今野 卓哉, 他田 正義, 岡崎 健一, 荒川 武蔵, 横尾 英明, 伊東 恭子, 吉倉 延亮, 豊島 靖子, 小野寺 理, 西澤 正豊, 池内 健, 高橋 均, 柿田 明美

    臨床神経学   53 ( 12 )   1529 - 1529   2013.12

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  • 神経軸索スフェロイドを伴う白質脳症HDLSの臨床・遺伝学的解析

    他田 正義, 今野 卓哉, 他田 真理, 荒川 武蔵, 小山 哲秀, 野崎 洋明, 針谷 康夫, 西宮 仁, 松永 晶子, 米田 誠, 吉倉 延亮, 犬塚 貴, 石原 健司, 河村 満, 高橋 均, 小野寺 理, 西澤 正豊, 池内 健

    臨床神経学   53 ( 12 )   1529 - 1529   2013.12

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  • 神経軸索スフェロイドを伴う白質脳症HDLSの病態解析 ハプロ不全とCSF1Rシグナル障害

    今野 卓哉, 他田 正義, 他田 真理, 小山 哲秀, 野崎 洋明, 高橋 均, 西澤 正豊, 小野寺 理, 柿田 明美, 池内 健

    Dementia Japan   27 ( 4 )   491 - 491   2013.10

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  • 神経軸索スフェロイドを伴う白質脳症HDLSの臨床・画像・遺伝学的解析

    他田 正義, 今野 卓哉, 他田 真理, 小山 哲秀, 野崎 洋明, 高橋 均, 西澤 正豊, 小野寺 理, 柿田 明美, 池内 健

    Dementia Japan   27 ( 4 )   490 - 490   2013.10

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  • HDLS(hereditary diffuse leukoencephalopathy with spheroids)のMRI所見

    今野 卓哉, 須貝 章弘, 西澤 正豊, 他田 正義, 小野寺 理, 他田 真理, 野崎 洋明, 小山 哲秀, 池内 健

    新潟医学会雑誌   127 ( 6 )   334 - 334   2013.6

  • Hereditary diffuse leukoencephalopathy with spheroids(HDLS)の臨床・病理・遺伝学的特徴

    他田 正義, 今野 卓哉, 他田 真理, 荒川 武蔵, 高橋 均, 小野寺 理, 西澤 正豊, 池内 健

    日本内科学会雑誌   102 ( Suppl. )   236 - 236   2013.2

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  • Corticobasal syndromeの臨床病理学的検討

    大内 東香, 下畑 享良, 豊島 靖子, 他田 真理, 高橋 均, 西澤 正豊

    臨床神経学   52 ( 12 )   1596 - 1596   2012.12

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  • 上位運動ニューロンの組織変性が下位のそれに比し高度であったALS剖検例の検討

    他田 真理, 柿田 明美, 志賀 篤, 黒羽 泰子, 小池 亮子, 樋口 真也, 森 茂, 付 永娟, 豊島 靖子, 小柳 清光, 西澤 正豊, 高橋 均

    臨床神経学   52 ( 12 )   1600 - 1600   2012.12

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  • パーキンソン病大脳皮質におけるアクアポリン発現の検討

    星 明彦, 角田 綾子, 宇川 義一, 西澤 正豊, 他田 真理, 柿田 明美, 高橋 均

    脳循環代謝   24 ( 1 )   222 - 222   2012.11

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  • 易疲労性、筋痛で発症し、T3271C点変異を有するミトコンドリア病19歳女性例の治療経験

    黒羽 泰子, 松原 奈絵, 長谷川 有香, 谷 卓, 他田 真理, 河内 泉, 西澤 正豊, 小池 亮子

    神経治療学   29 ( 5 )   653 - 653   2012.9

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  • Clinicopathological Analysis of Japanese Patients with Corticobasal Syndrome

    Haruka Ouchi, Takayoshi Shimohata, Yasuko Toyoshima, Mari Tada, Hitoshi Takahashi, Masatoyo Nishizawa

    NEUROLOGY   78   2012.4

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  • ハンチントン病とALS合併例の臨床病理学的検討

    他田 真理, Coon Elizabeth, Osmand Alexander, Kirby Patricia, Martin Wayne, Wieler Marguerite, Paulson Henry

    臨床神経学   51 ( 12 )   1436 - 1436   2011.12

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  • ヒト疾患脳におけるポリグルタミン病重合体の検出

    高橋 俊昭, 石平 悠, 堅田 慎一, 他田 正義, 他田 真理, 佐藤 俊哉, 柿田 明美, 高橋 均, 小野寺 理, 西澤 正豊

    臨床神経学   51 ( 12 )   1272 - 1272   2011.12

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  • 臨床医のための神経病理 多系統萎縮症の自律神経病理 生命維持に関わる領域 Invited

    小澤 鉄太郎, 他田 真理, 西澤 正豊

    Clinical Neuroscience   29 ( 9 )   974 - 975   2011.9

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  • Coexistence of Huntington&apos;s Disease and Amyotrophic Lateral Sclerosis: Clinicopathologic Study

    Mari Tada, Elizabeth A. Coon, Alexander P. Osmand, Patricia A. Kirby, Wayne Martin, Marguerite Wieler, Henry Paulson

    NEUROLOGY   76 ( 9 )   A588 - A589   2011.3

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  • Disequilibrium in MSA phenotype distribution between populations: genetics or environment?

    T. Ozawa, J. L. Holton, D. Paviour, A. J. Lees, M. Tada, A. Kakita, O. Onodera, K. Wakabayashi, H. Takahashi, M. Nishizawa, T. Revesz

    BRAIN PATHOLOGY   20   29 - 29   2010.9

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  • 日本人MSA剖検例の表現型スペクトラム 英国の結果と対比して

    小澤 鉄太郎, 他田 真理, 小野寺 理, 柿田 明美, 高橋 均, 西澤 正豊

    臨床神経学   49 ( 12 )   1133 - 1133   2009.12

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  • The spectrum of pathological involvement in Japanese patients with multiple system atrophy: A population-bound phenotype distribution

    T. Ozawa, M. Tada, O. Onodera, A. Kakita, T. Shimohata, H. Takahashi, N. Nishizawa

    MOVEMENT DISORDERS   24   S416 - S417   2009

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  • 進行性核上性麻痺の臨床病型の検討

    金澤 雅人, 下畑 享良, 柿田 明美, 豊島 靖子, 他田 真理, 森田 俊, 高橋 均, 西澤 正豊

    臨床神経学   47 ( 12 )   1059 - 1059   2007.12

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  • 血管内悪性リンパ腫に類似したMRI画像を呈したが、リンパ腫様肉芽腫症と考えられた一症例

    石原 聡, 花城 清祥, 崎山 佑介, 延原 康幸, 諏訪園 秀吾, 他田 真理, 高橋 均, 末原 雅人

    臨床神経学   47 ( 2-3 )   125 - 125   2007.3

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  • Multiple system atrophy: Morphometric evaluation of the CNS autonomic nuclei in patients with sudden deaths

    Mari Tada, Akiyoshi Kakita, Osamu Onodera, Masatoyo Nishizawa, Hitoshi Takahashi

    NEUROLOGY   68 ( 12 )   A50 - A50   2007.3

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  • Chronic myositis with cardiomyopathy and respiratory failure associated with mild form of organ-specific autoimmune diseases

    K.Tanaka, Sato A, Kasuga K, Kanazawa M, Yanagawa K, Umeda M, Tada M, Tanaka M, Nishizawa M

    Clin Rheumatol   26   1917–1919   2007

  • 神経変性疾患の鑑別診断のための脳血流SPECT画像の情報の縮約方法の検討

    中島 孝, 亀井 啓史, 川上 英孝, 米持 洋介, 他田 真理, 林 恒美

    臨床神経学   46 ( 12 )   1145 - 1145   2006.12

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  • 多系統萎縮症における睡眠時声門閉鎖率と嚥下障害の臨床的相関

    小澤 鉄太郎, 篠田 秀夫, 大瀧 祥子, 下畑 享良, 寺島 健史, 谷口 裕重, 他田 真理, 他田 正義, 横関 明男, 新保 淳輔, 五十嵐 修一, 小野寺 理, 田中 恵子, 西澤 正豊

    臨床神経学   46 ( 12 )   1083 - 1083   2006.12

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  • Marinesco-Sjogren症候群の臨床病理学的検討

    米持 洋介, 亀井 啓史, 会田 泉, 伊藤 博明, 川上 英孝, 中島 孝, 坂井 健二, 他田 真理, 高橋 均

    臨床神経学   46 ( 12 )   1169 - 1169   2006.12

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  • 多系統萎縮症早期死亡例の臨床病理学的検討

    他田 真理, 柿田 明美, 小野寺 理, 西澤 正豊, 高橋 均

    臨床神経学   46 ( 12 )   1134 - 1134   2006.12

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  • Marinesco-Sjoegren症候群と考えられた1剖検例

    坂井 健二, 他田 真理, 高橋 均, 米持 洋介

    信州医学雑誌   54 ( 4 )   239 - 240   2006.8

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  • 脳生検にて確診されたprogressive multifocal leukoencephalopathyの1例

    他田 真理, 西平 靖, 池田 哲彦, 眞野 篤, 小澤 鉄太郎, 西澤 正豊, 高橋 均

    信州医学雑誌   54 ( 4 )   238 - 239   2006.8

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  • Multiple system atrophy: Morphometric evaluation of the CNS autonomic nuclei in patients with sudden deaths

    M. Tada, A. Kakita, O. Onodera, M. Nishizawa, H. Takahashi

    MOVEMENT DISORDERS   21   S535 - S535   2006

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  • Patient with adult-onset congenital neuromuscular disease

    T. Shimohata, H. Sano, Y.Takado, M. Tada, K.Tanaka, M.Nishizawa

    European Journal of Neurology   13   1468 - 1331   2006

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  • 多系統萎縮症における睡眠時声門閉鎖率解析

    小澤 鉄太郎, 篠田 秀夫, 中山 秀章, 下畑 享良, 寺島 健史, 他田 真理, 他田 正義, 横関 明男, 新保 淳輔, 五十嵐 修一, 小野寺 理, 田中 恵子, 西澤 正豊

    臨床神経学   45 ( 12 )   1166 - 1166   2005.12

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  • 進行性筋萎縮症における下肢深部静脈血栓症

    川上 英孝, 中島 孝, 亀井 啓史, 他田 真理, 米持 洋介, 榛沢 和彦

    臨床神経学   45 ( 12 )   1138 - 1138   2005.12

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  • 病理学的に確認された多系統萎縮症49例の臨床像の検討

    他田 真理, 小野寺 理, 小澤 鉄太郎, 他田 正義, 朴 月善, 高橋 均, 西澤 正豊

    臨床神経学   45 ( 12 )   1167 - 1167   2005.12

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  • 脳血流SPECTの判別分析法に基づくパーキンソニズムの診断アルゴリズム

    中島 孝, 亀井 啓史, 川上 英孝, 米持 洋介, 他田 真理, 林 恒美

    臨床神経学   45 ( 12 )   1193 - 1193   2005.12

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  • The trouble with eponyms - In reply

    M Tada, M Tada, H Ishiguro, K Hirota

    ARCHIVES OF NEUROLOGY   62 ( 11 )   1785 - 1785   2005.11

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  • The trouble with eponyms [1] (multiple letters)

    Henry S. Schutta, Masayoshi Tada, Mari Tada, Hideaki Ishiguro, Kouichi Hirota

    Archives of Neurology   62 ( 11 )   1784 - 1785   2005.11

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    DOI: 10.1001/archneur.62.11.1784

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  • 高齢で発症したCongenital neuromuscular disease with uniform type 1 fibersの1例

    佐野 博繁, 下畑 享良, 他田 真理, 田中 恵子, 西澤 正豊

    臨床神経学   45 ( 1 )   53 - 53   2005.1

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  • 全身型重症筋無力症に対するタクロリムス(プログラフ)の当科使用成績

    他田 正義, 下畑 享良, 他田 真理, 成瀬 聡, 田中 恵子, 辻 省次, 西澤 正豊

    臨床神経学   44 ( 12 )   1207 - 1207   2004.12

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  • 明らかな家族歴をもたない眼咽頭筋ジストロフィーの1例

    徳武 孝允, 池内 健, 他田 真理, 田中 惠子, 西澤 正豊

    臨床神経学   44 ( 8 )   556 - 556   2004.8

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  • 切迫脳ヘルニアをきたした非ヘルペス性急性髄膜脳炎にたいする脳低体温療法の試み

    富樫 優, 寺島 健史, 他田 真理, 成瀬 聡, 田中 惠子, 西澤 正豊

    神経治療学   21 ( 3 )   278 - 278   2004.5

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  • HAMで発症し約18年後にATLを発症,死亡した1例

    石黒 英明, 他田 正義, 他田 真理, 小出 隆司, 廣田 紘一, 斉藤 謙, 吉田 泰二

    臨床神経学   44 ( 1 )   71 - 71   2004.1

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  • 重篤な多発性単ニューロパチーを呈し,C型肝炎ウィルス感染に関連した混合型クリオグロブリン血症をみとめた全身性血管炎の1剖検例

    他田真理, 成瀬 聡, 新井 亜希, 佐藤 晶, 田中惠子, 朴 月善, 柿田明美, 高橋 均, 西澤正豊, 辻 省次

    臨床神経   44   686 - 690   2004

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  • Clinical features of 49 pathologically proven multiple system atrophy in the Japanese population

    M Tada, T Ozawa, O Onodera, M Tada, H Takahashi, M Nishizawa

    MOVEMENT DISORDERS   19   S24 - S24   2004

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    Web of Science

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  • 原発巣不明の癌性髄膜炎の一例

    石黒 英明, 小出 隆司, 他田 正義, 他田 真理, 新保 淳輔, 斎藤 謙

    日赤医学   55 ( 1 )   266 - 266   2003.9

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  • Eczematous Reactions after Intravenous Immunoglobulin Therapy in Two Patients with Guillain-Barre Syndrome and a Patient with Miller Fisher Syndrome

    55 ( 5 )   401 - 405   2003.5

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  • Two cases of lumhosacral radiculopathy after intra-arterial infusion of cisplatin for treatment of uterine cancer

    HARA Kenju, TADA Mari, NARUSE Satoshi, SOMA Yoshiaki, KOJIMA Yumi, KURATA Hitoshi, TANAKA Kenichi, TSUJI Shoji

    43 ( 1〜2 )   26 - 30   2003.1

  • Consciousness Disturbance Caused by Iodoform Absorption in a Patient with Decubitus Ulcer Topically Treated with Iodoform-Gauze

    54 ( 12 )   1051 - 1054   2002.12

  • Intravascular large B-cell lymphomaの剖検例

    石黒 英明, 他田 正義, 他田 真理, 小出 隆司, 新保 淳輔, 斉藤 謙, 廣田 紘一, 吉田 泰二

    臨床神経学   42 ( 7 )   647 - 647   2002.7

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  • 三叉神経障害で発症し,両側メッケル腔の病変と胸部リンパ節腫脹を認めた1例

    他田 真理, 他田 正義, 石黒 英明, 廣田 紘一

    臨床神経学   42 ( 1 )   78 - 78   2002.1

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  • 当院における一酸化炭素中毒に対する高圧酸素療法

    永井 博子, 他田 真理, 藤田 信也

    臨床神経学   41 ( 11 )   918 - 918   2001.11

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  • 大量免疫グロブリン静注療法(IVIG)後に類似の水疱・血疱が生じた3症例

    他田 正義, 他田 真理, 石黒 英明, 廣田 紘一, 八木 英一

    臨床神経学   41 ( 7 )   451 - 451   2001.7

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  • 妊娠後期の感染症状を契機に全身性紅斑,急性腎不全,両側性顔面神経麻痺を呈し,良好な経過をとった1例

    他田 正義, 他田 真理, 石黒 英明, 廣田 紘一

    臨床神経学   41 ( 7 )   456 - 456   2001.7

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  • 生体肝移植で神経症状の改善を認めたウイルソン病の1例

    藤田 信也, 他田 真理, 永井 博子, 五十川 修, 川村 邦雄, 成瀬 聡, 辻 省次, 佐藤 好信

    臨床神経学   41 ( 6 )   340 - 340   2001.6

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  • 70歳で発症し,ステロイドとアザチオプリンの併用療法で良好な経過をたどった多発性硬化症(Devic病)の一例

    丸山 正樹, 藤田 信也, 他田 真理, 永井 博子

    臨床神経学   41 ( 4〜5 )   247 - 247   2001.4

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  • 健常者にみられたクリプトコッカス髄膜脳炎の1例

    他田 真理, 藤田 信也, 永井 博子

    臨床神経学   41 ( 1 )   80 - 80   2001.1

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  • 抗GQ1b抗体症候群の臨床の多様性

    藤田 信也, 他田 真理, 永井 博子, 吉野 英

    日赤医学   52 ( 1 )   117 - 117   2000.10

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  • HCV関連II型クリオグロブリン血症を伴う血管炎による高度末梢神経障害の1例

    他田 真理, 成瀬 聡, 田中 恵子, 相馬 芳明, 辻 省次

    臨床神経学   40 ( 5 )   519 - 519   2000.5

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  • HCCを合併した自己免疫性肝炎と考えられる1例

    他田 真理, 田口 澄人, 八木 一芳, 後藤 俊夫, 大原 一彦, 小田 栄司, 櫻井 金三, 関根 厚雄, 阿部 道行, 飯泉 俊雄

    新潟医学会雑誌   114 ( 4 )   166 - 167   2000.4

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    Other Link: http://search.jamas.or.jp/link/ui/2000238932

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Presentations

  • 脱髄・白質脳症 Invited

    他田真理

    第60回日本神経病理学会総会学術研究会  2019.7 

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    Event date: 2019.7

    Language:Japanese   Presentation type:Symposium, workshop panel (nominated)  

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  • Adult-onset leukoencephalopathy with axonal spheroids and pigmented glia (ALSP): pathologic features suggestive of microgliopathy Invited International conference

    Mari Tada, Akiyoshi Kakita

    19th International Congress of Neuropathology  2018.9 

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  • 神経軸索スフェロイドを伴う遺伝性びまん性白質脳症(HDLS)の臨床と病理 Invited

    他田 真理, 柿田明美

    第59回日本神経学会学術大会  2018.5 

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  • 認知症を呈する白質脳症におけるグリア細胞の関与 Invited

    他田 真理, 柿田明美

    第36回日本認知症学会学術集会  2017.11 

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  • Hereditary diffuse leukoencephalopathy with spheroids (HDLS) 患者脳におけるミクログリアの形態学的異常:Microgliopathyとして Invited

    他田 真理, 柿田明美

    第56回日本神経学会学術大会  2015.5 

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Awards

  • 第55回総会学術研究会優秀ポスター賞

    日本神経病理学会  

    他田 真理

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Research Projects

  • 認知症治療標的としてのミクログリアによるアストロサイト制御機構に剖検脳から迫る

    Grant number:22H02995  2022.4 - 2025.3

    日本学術振興会  科学研究費助成事業 基盤研究(B)  基盤研究(B)

    他田 真理

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    Grant amount:\17680000 ( Direct Cost: \13600000 、 Indirect Cost:\4080000 )

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  • 白質脳症におけるミクログリアによるアストロサイトの制御機構

    Grant number:19K07972  2019.4 - 2022.3

    日本学術振興会  科学研究費助成事業 基盤研究(C)  基盤研究(C)

    他田 真理, 池内 健, 竹林 浩秀, 加藤 隆弘, 柿田 明美

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    Grant amount:\4420000 ( Direct Cost: \3400000 、 Indirect Cost:\1020000 )

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  • ミクログリアの異常がなぜ白質変性をきたすのか

    2016.4 - 2019.3

    日本学術振興会  科学研究費基盤研究(C) 

    他田 真理

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    Authorship:Principal investigator  Grant type:Competitive

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  • 多系統萎縮症における認知機能障害の責任病巣:臨床病理学的検討

    2013.4 - 2016.3

    日本学術振興会  科学研究費基盤研究(C) 

    他田 真理

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Teaching Experience (researchmap)

  • 神経病理学

    Institution name:新潟大学医学部

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