Updated on 2024/04/23

写真a

 
SAITO Rie
 
Organization
Brain Research Institute Center for Bioresources Assistant Professor
Title
Assistant Professor
External link

Degree

  • Doctor (Neuropathology) ( 2018.3   Niigata University )

Research Interests

  • 脳血管障害

  • Neuropathology

  • Neurodegenerative disease

  • 血管性認知症

  • 白質脳症

Research Areas

  • Life Science / Anatomy and histopathology of nervous system

  • Life Science / Neurology

Research History (researchmap)

  • Niigata University   Brain Research Institute   Assistant Professor

    2018.4

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  • Niigata University   Graduate School of Medical and Dental Sciences

    2014.4 - 2018.3

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  • 国家公務員共済組合連合会虎の門病院   神経内科   医員

    2012.4 - 2014.3

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  • 国家公務員共済組合連合会虎の門病院   内科   後期専門研修（神経内科専攻）

    2009.4 - 2012.3

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  • 国家公務員共済組合連合会虎の門病院   内科   初期研修

    2007.4 - 2009.3

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Research History

  • Niigata University   Center for Bioresources, Brain Research Institute   Assistant Professor

    2023.4

  • Niigata University   Brain Research Institute   Assistant Professor

    2018.4 - 2023.3

Education

  • Niigata University   Faculty of Medicine   School of Medicine

    2007.3

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Professional Memberships

Committee Memberships

  • The Japanese Society of Neuropathology   Councilor of the International Congress of Neuropathology  

    2024.4   

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  • 日本神経病理学会   将来計画委員／用語委員／基礎臨床連携促進委員会  

    2021.4   

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  • 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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Qualification acquired

  • 神経内科専門医

 

Papers

  • Clinicopathologic features of two unrelated autopsied patients with Charcot-Marie-Tooth disease carrying MFN2 gene mutation Reviewed

    Hideki Hayashi, Rie Saito, Hidetomo Tanaka, Norikazu Hara, Shin Koide, Yosuke Yonemochi, Tetsuo Ozawa, Mariko Hokari, Yasuko Toyoshima, Akinori Miyashita, Osamu Onodera, Kouichirou Okamoto, Takeshi Ikeuchi, Takashi Nakajima, Akiyoshi Kakita

    Acta Neuropathologica Communications   2023.12

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

    DOI： 10.1186/s40478-023-01692-w

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  • Marked laterality of olivopontocerebellar pathology in an autopsied patient with MSA: Implications for degeneration and α-synuclein propagation. Reviewed International journal

    Misato Ozawa, Rie Saito, Takuya Konno, Reiji Koide, Shigeru Fujimoto, Osamu Onodera, Akiyoshi Kakita

    Journal of neurology, neurosurgery, and psychiatry   2023.11

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    Authorship：Corresponding author   Language：English  

    DOI： 10.1136/jnnp-2023-332419

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  • V180I genetic Creutzfeldt-Jakob disease: Severe degeneration of the inferior olivary nucleus in an autopsied patient with identification of the M2T prion strain. Reviewed International journal

    Midori Watanabe, Kosei Nakamura, Rie Saito, Atsuko Takeuchi, Tetsuya Takahashi, Tetsuyuki Kitamoto, Osamu Onodera, Akiyoshi Kakita

    Neuropathology : official journal of the Japanese Society of Neuropathology   2023.5

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    Authorship：Corresponding author   Language：English  

    Genetic Creutzfeldt-Jakob disease (gCJD) with a V180I mutation (V180I gCJD) is the most common type of gCJD in Japan, characterized by an older age at onset, slower progression, and moderate to severe cortical degeneration with spongiform changes and sparing of the brainstem and cerebellum. Degeneration of the inferior olivary nucleus (IO) is rarely observed in patients with CJD but is known to occur in fatal familial insomnia (FFI) and MM2-thalamic-type sporadic CJD (sCJD-MM2T) involving type 2 prion protein (M2T prion). Here we report on an 81-year-old Japanese woman who initially developed depressive symptoms followed by progressive cognitive impairment, myoclonus, and hallucinations and died after a clinical course of 23 months. Insomnia was not evident. Genetic analysis of the prion protein (PrP) identified a V180I mutation with methionine/valine heterozygosity at codon 129. Pathologic analysis demonstrated extensive spongiform degeneration, neuronal loss in the cortices, and weak synaptic-type PrP deposition. Except for IO degeneration, the clinicopathologic features and Western blotting PrP band pattern were compatible with those of previously reported V180I gCJD cases. Quantitative analysis revealed that the neuronal density of the IO, especially in the dorsal area, was considerably reduced to the same extent as that of a patient with sCJD-MM2T but preserved in other patients with V180I gCJD and sCJD-MM1 (this patient, 2.3 ± 0.53/mm2 ; a patient with sCJD-MM2T, 4.2 ± 2; a patient with V180I gCJD, 60.5 ± 9.3; and a patient with sCJD-MM1, 84.5 ± 17.9). Use of the protein misfolding cyclic amplification (PMCA) method confirmed the presence of the M2T prion strain, suggesting that the latter might be associated with IO degeneration in V180I gCJD. Autopsy studies are necessary to better understand the nature of CJD, since even if patients present with the common clinical picture, pathologic analysis might provide new insights, as was the case here.

    DOI： 10.1111/neup.12908

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  • SYNE1-ataxia: clinicopathologic features of an autopsied patient with novel compound heterozygous mutations Reviewed

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

    Journal of Neuropathology & Experimental Neurology   2023.2

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

    DOI： 10.1093/jnen/nlac120

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  • Spinocerebellar ataxia type 17-digenic TBP/STUB1 disease: neuropathologic features of an autopsied patient Reviewed International journal

    Rie Saito, Yui Tada, Daisuke Oikawa, Yusuke Sato, Makiko Seto, Akira Satoh, Kodai Kume, Nozomi Ueki, Masahiro Nakashima, Shintaro Hayashi, Yasuko Toyoshima, Fuminori Tokunaga, Hideshi Kawakami, Akiyoshi Kakita

    Acta Neuropathologica Communications   10 ( 1 )   177 - 177   2022.12

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    Authorship：Lead author   Language：English   Publishing type：Research paper (scientific journal)   Publisher：Springer Science and Business Media LLC  

    Abstract

    Spinocerebellar ataxia (SCA) type 17-digenic TBP/STUB1 disease (SCA17-DI) has been recently segregated from SCA17, caused by digenic inheritance of two gene mutations – intermediate polyglutamine-encoding CAG/CAA repeat expansions (polyQ) in TBP (TBP<sub>41 − 49</sub>) and STUB1 heterozygosity – the former being associated with SCA17, and the latter with SCA48 and SCAR16 (autosomal recessive). In SCA17, most patients carry intermediate TBP<sub>41 − 49</sub> alleles but show incomplete penetrance, and the missing heritability can be explained by a new entity whereby TBP<sub>41 − 49</sub> requires the STUB1 variant to be symptomatic. The STUB1 gene encodes the chaperone-associated E3 ubiquitin ligase (CHIP) involved in ubiquitin-mediated proteasomal control of protein homeostasis. However, reports of the neuropathology are limited and role of STUB1 mutations in SCA17-DI remain unknown. Here we report the clinicopathologic features of identical twin siblings, one of whom was autopsied and was found to carry an intermediate allele (41 and 38 CAG/CAA repeats) in TBP and a heterozygous missense mutation in STUB1 (p.P243L). These patients developed autosomal recessive Huntington’s disease-like symptoms. Brain MRI showed diffuse atrophy of the cerebellum and T2WI revealed hyperintense lesions in the basal ganglia and periventricular deep white matter. The brain histopathology of the patient shared features characteristic of SCA17, such as degeneration of the cerebellar cortex and caudate nucleus, and presence of 1C2-positive neurons. Here we show that mutant CHIP fails to generate the polyubiquitin chain due to disrupted folding of the entire U box domain, thereby affecting the E3 activity of CHIP. When encountering patients with cerebellar ataxia, especially those with Huntington’s disease-like symptoms, genetic testing for STUB1 as well as TBP should be conducted for diagnosis of SCA17-DI, even in cases of sporadic or autosomal recessive inheritance.

    DOI： 10.1186/s40478-022-01486-6

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    Other Link： https://link.springer.com/article/10.1186/s40478-022-01486-6/fulltext.html

  • Candesartan prevents arteriopathy progression in cerebral autosomal recessive arteriopathy with subcortical infarcts and leukoencephalopathy model. Reviewed International journal

    Taisuke Kato, Ri-Ichiroh Manabe, Hironaka Igarashi, Fuyuki Kametani, Sachiko Hirokawa, Yumi Sekine, Natsumi Fujita, Satoshi Saito, Yusuke Kawashima, Yuya Hatano, Shoichiro Ando, Hiroaki Nozaki, Akihiro Sugai, Masahiro Uemura, Masaki Fukunaga, Toshiya Sato, Akihide Koyama, Rie Saito, Atsushi Sugie, Yasuko Toyoshima, Hirotoshi Kawata, Shigeo Murayama, Masaki Matsumoto, Akiyoshi Kakita, Masato Hasegawa, Masafumi Ihara, Masato Kanazawa, Masatoyo Nishizawa, Shoji Tsuji, Osamu Onodera

    The Journal of clinical investigation   131 ( 22 )   2021.11

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    Language：English   Publishing type：Research paper (scientific journal)  

    Cerebral small vessel disease (CSVD) causes dementia and gait disturbance due to arteriopathy. Cerebral autosomal recessive arteriopathy with subcortical infarcts and leukoencephalopathy (CARASIL) is a hereditary form of CSVD caused by loss of high-temperature requirement A1 (HTRA1) serine protease activity. In CARASIL, arteriopathy causes intimal thickening, smooth muscle cell (SMC) degeneration, elastic lamina splitting, and vasodilation. The molecular mechanisms were proposed to involve the accumulation of matrisome proteins as substrates or abnormalities in transforming growth factor β (TGF-β) signaling. Here, we show that HTRA1-/- mice exhibited features of CARASIL-associated arteriopathy: intimal thickening, abnormal elastic lamina, and vasodilation. In addition, the mice exhibited reduced distensibility of the cerebral arteries and blood flow in the cerebral cortex. In the thickened intima, matrisome proteins, including the hub protein fibronectin (FN) and latent TGF-β binding protein 4 (LTBP-4), which are substrates of HTRA1, accumulated. Candesartan treatment alleviated matrisome protein accumulation and normalized the vascular distensibility and cerebral blood flow. Furthermore, candesartan reduced the mRNA expression of Fn1, Ltbp-4, and Adamtsl2, which are involved in forming the extracellular matrix network. Our results indicate that these accumulated matrisome proteins may be potential therapeutic targets for arteriopathy in CARASIL.

    DOI： 10.1172/JCI140555

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  • Long Spinal Cord Lesions Caused by Venous Congestive Myelopathy Associated with Intravascular Large B-cell Lymphoma. Reviewed

    Takeshi Miura, Shoji Saito, Rie Saito, Tomohiro Iwasaki, Naomi Mezaki, Tomoe Sato, Yoichi Ajioka, Akiyoshi Kakita, Takuya Mashima

    Internal medicine (Tokyo, Japan)   2021.6

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    Language：English   Publishing type：Research paper (scientific journal)  

    Intravascular large B-cell lymphoma (IVLBCL) is a subtype of B-cell lymphoma, characterized by lymphoma cell proliferation within small blood vessels. We herein describe a rare case with long spinal cord lesions caused by venous congestive myelopathy associated with IVLBCL. An 81-year-old man presented with paraplegia of the lower limbs and sensory disturbances. Magnetic resonance imaging revealed intramedullary longitudinal T2-hyperintensity lesions in the thoracic cords. The patient died three months after disease onset, and a neuropathological analysis revealed predominantly atypical B-lymphocytes located sparsely in the veins of the spinal cord. IVLBCL should be considered in the differential diagnoses of long spinal cord lesions.

    DOI： 10.2169/internalmedicine.6717-20

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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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    Authorship：Lead author,　Corresponding author   Language：English  

    DOI： 10.1186/s40478-020-01008-2

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  • Oculopharyngodistal myopathy with coexisting histology of systemic neuronal intranuclear inclusion disease: Clinicopathologic features of an autopsied patient harboring CGG repeat expansions in LRP12. Reviewed International journal

    Rie Saito, Hiroshi Shimizu, Takeshi Miura, Norikazu Hara, Naomi Mezaki, Yo Higuchi, Akinori Miyashita, Izumi Kawachi, Kazuhiro Sanpei, Yoshiaki Honma, Osamu Onodera, Takeshi Ikeuchi, Akiyoshi Kakita

    Acta neuropathologica communications   8 ( 1 )   75 - 75   2020.6

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    Authorship：Lead author   Language：English  

    DOI： 10.1186/s40478-020-00945-2

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  • Dramatic response of BRAF V600E-mutant epithelioid glioblastoma to combination therapy with BRAF and MEK inhibitor: establishment and xenograft of a cell line to predict clinical efficacy. Reviewed International journal

    Kanemaru Y, Natsumeda M, Okada M, Saito R, Kobayashi D, Eda T, Watanabe J, Saito S, Tsukamoto Y, Oishi M, Saito H, Nagahashi M, Sasaki T, Hashizume R, Aoyama H, Wakai T, Kakita A, Fujii Y

    Acta neuropathologica communications   7 ( 1 )   119 - 119   2019.7

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    Language：English   Publishing type：Research paper (scientific journal)  

    Epithelioid glioblastoma is a rare aggressive variant of glioblastoma (GBM) characterized by a dismal prognosis of about 6 months and frequent leptomeningeal dissemination. A recent study has revealed that 50% of epithelioid GBMs harbor three genetic alterations - BRAF V600E mutation, TERT promoter mutations, and homozygous deletions of CDKN2A/2B. Emerging evidence support the effectiveness of targeted therapies for brain tumors with BRAF V600E mutation. Here we describe a dramatic radiographical response to combined therapy with BRAF and MEK inhibitors in a patient with epithelioid GBM harboring BRAF V600E mutation, characterized by thick spinal dissemination. From relapsed tumor procured at autopsy, we established a cell line retaining the BRAF V600E mutation, TERT promoter mutation and CDKN2A/2B loss. Intracranial implantation of these cells into mice resulted in tumors closely resembling the original, characterized by epithelioid tumor cells and dissemination, and invasion into the perivascular spaces. We then confirmed the efficacy of treatment with BRAF and MEK inhibitor both in vitro and in vivo. Epithelioid GBM with BRAF V600E mutation can be considered a good treatment indication for precision medicine, and this patient-derived cell line should be useful for prediction of the tumor response and clarification of its biological characteristics.

    DOI： 10.1186/s40478-019-0774-7

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  • Rapid chemical clearing of white matter in the post-mortem human brain by 1,2-hexanediol delipidation. Reviewed

    Rie Saito

    Bioorganic & medicinal chemistry letters   29 ( 15 )   1886 - 1890   2019.5

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    Publishing type：Research paper (scientific journal)  

    Three-dimensional (3D) imaging based on chemical tissue clearing in the post-mortem human brain is a promising approach for stereoscopic understanding of central nervous system diseases. Especially, delipidation of lipid-rich white matter (WM) is a rate-determining step in human brain clearing by hydrophilic reagents. In this study, we described the rapid delipidation of WM by a 1,2-hexanediol (HxD)-based aqueous solution. HxD delipidation enabled rapid clearing of a formalin-fixed human brain specimen including the WM. Although harsh HxD delipidation was applied to the brain tissue, conventional pathological staining patterns and various types of antigenicity were sufficiently preserved. Furthermore, HxD delipidation was compatible with 3D imaging of fluorescently-labeled tissue samples. HxD delipidation could be useful in future 3D neuropathological diagnosis.

    DOI： 10.1016/j.bmcl.2019.05.049

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  • Retinal Vasculopathy With Cerebral Leukodystrophy: Clinicopathologic Features of an Autopsied Patient With a Heterozygous TREX 1 Mutation. Reviewed

    Rie Saito

    Journal of neuropathology and experimental neurology   2019.2

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    Authorship：Lead author   Publishing type：Research paper (scientific journal)  

    Retinal vasculopathy with cerebral leukodystrophy (RVCL) is an autosomal-dominant disorder involving the cerebral, retinal, renal, and other systemic microvessels due to frameshift mutations in the TREX1 gene. Under physiological conditions, the TREX1 protein is localized in the cellular cytoplasm and perinuclear area, but translocates into the nucleus in response to oxidative DNA damage. It has been speculated that aberrant localization of the protein may be associated with systemic microangiopathy in patients with RVCL. However, cellular expression of TREX1 in the brain and visceral organs of patients with RVCL has been unclear. Here, we report the clinicopathologic features of an autopsied patient with a heterozygous T249fs mutation in TREX1. The patient showed the clinical phenotype of vasculopathy with retinopathy, nephropathy, and stroke. CT with contrast enhancement demonstrated a tumorous lesion in the subcortical white matter. Histologically, the lesion consisted of confluent foci of necrosis with calcification and fibrous thickening of small vessel walls. TREX1 immunohistochemistry demonstrated positivity in the nuclei of cells in the CNS and visceral organs, indicating aberrant localization of the truncated protein, and the expression was remarkable in oligodendrocytes within the lesion, suggesting possible involvement of the protein in the pathomechanism of vasculopathy leading to white matter degeneration.

    DOI： 10.1093/jnen/nly115

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  • Chemical Landscape for Tissue Clearing Based on Hydrophilic Reagents. Reviewed International journal

    Kazuki Tainaka, Tatsuya C Murakami, Etsuo A Susaki, Chika Shimizu, Rie Saito, Kei Takahashi, Akiko Hayashi-Takagi, Hiroshi Sekiya, Yasunobu Arima, Satoshi Nojima, Masako Ikemura, Tetsuo Ushiku, Yoshihiro Shimizu, Masaaki Murakami, Kenji F Tanaka, Masamitsu Iino, Haruo Kasai, Toshikuni Sasaoka, Kazuto Kobayashi, Kohei Miyazono, Eiichi Morii, Tadashi Isa, Masashi Fukayama, Akiyoshi Kakita, Hiroki R Ueda

    Cell reports   24 ( 8 )   2196 - 2210   2018.8

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    Language：English   Publishing type：Research paper (scientific journal)  

    We describe a strategy for developing hydrophilic chemical cocktails for tissue delipidation, decoloring, refractive index (RI) matching, and decalcification, based on comprehensive chemical profiling. More than 1,600 chemicals were screened by a high-throughput evaluation system for each chemical process. The chemical profiling revealed important chemical factors: salt-free amine with high octanol/water partition-coefficient (logP) for delipidation, N-alkylimidazole for decoloring, aromatic amide for RI matching, and protonation of phosphate ion for decalcification. The strategic integration of optimal chemical cocktails provided a series of CUBIC (clear, unobstructed brain/body imaging cocktails and computational analysis) protocols, which efficiently clear mouse organs, mouse body including bone, and even large primate and human tissues. The updated CUBIC protocols are scalable and reproducible, and they enable three-dimensional imaging of the mammalian body and large primate and human tissues. This strategy represents a future paradigm for the rational design of hydrophilic clearing cocktails that can be used for large tissues.

    DOI： 10.1016/j.celrep.2018.07.056

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  • Renal histopathological findings of retinal vasculopathy with cerebral leukodystrophy. Reviewed

    Tsubata Y, Morita T, Morioka T, Sasagawa T, Ikarashi K, Saito N, Shimada H, Miyazaki S, Sakai S, Tanaka H, Saito R, Toyoshima Y, Nozaki H, Narita I

    CEN case reports   7 ( 1 )   83 - 89   2018.5

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

    Rie Saito

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

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    Authorship：Lead author   Publishing type：Research paper (scientific journal)  

    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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  • Nonfunctional intra- and suprasellar tumor in a patient with visual disturbance and panhypopituitarism. Reviewed

    Rie Saito

    Neuropathology : official journal of the Japanese Society of Neuropathology   36 ( 1 )   107 - 112   2015.8

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    Authorship：Lead author   Publishing type：Research paper (scientific journal)  

    DOI： 10.1111/neup.12236

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  • [A case of 77-year-old male with spinocerebellar ataxia type 31 with left dominant dystonia]. Reviewed

    Rie Saito, Shota Kikuno, Meiko Maeda, Yoshikazu Uesaka, Masahiro Ida

    Rinsho shinkeigaku = Clinical neurology   54 ( 8 )   643 - 7   2014

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    Authorship：Lead author   Language：Japanese   Publishing type：Research paper (scientific journal)  

    We report on the case of a 77-year-old male with genetically proven spinocerebellar ataxia type 31 (SCA31) who had dystonia. He was referred to our hospital for evaluation following a 6-year history of slowly progressive unsteadiness of his left leg during walking and dysarthria at the age of 62 years old. On the basis of his symptoms, we diagnosed him as spinocerebellar degeneration (SCD), and prescribed taltirelin hydrate. However, his symptoms continued to worsen. He required a cane for walking at the age of 63 years, and a wheelchair at the age of 66 years. He was admitted to our hospital following acute cerebral infarction at the age of 77 years. On examination at admission, right hemiparesis and cerebellar ataxia were detected. And left hallux moved involuntarily toward the top surface of the foot at rest, that is dystonia. The dystonia was not associated with cerebral infarction, because it had been several years with dystonia that he got cerebral infarction. Genetic analysis revealed that this patient harbored a heterozygous SCA31 mutation. Previously there have been no reports of SCA31 associated with dystonia. Our case report support clinical heterogeneity of SCA31, and highlight the importance of considering this type in patients with dystonia and ataxia. Patients with the combination of dystonia and ataxia and a family history of a neurodegenerative disorder should be tested for SCA31.

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MISC

  • An autopsied patient with palatal tremor and fatal bilateral vocal cord abduction paralysis associated with bilateral cerebellar dentate nucleus infarction Reviewed

    Tomoe Sato, Rie Saito, Makoto Sainouchi, Naomi Mezaki, Takeshi Miura, Takuya Mashima, Akiyoshi Kakita

    Rinsho Shinkeigaku   2023.8

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    Publisher：Societas Neurologica Japonica  

    DOI： 10.5692/clinicalneurol.cn-001859

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  • 【神経核内封入体病・白質脳症】脳小血管病の病理

    齋藤 理恵, 柿田 明美

    脳神経内科   97 ( 1 )   81 - 90   2022.7

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    Language：Japanese   Publisher：(有)科学評論社  

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  • 臨床医のための神経病理再入門 CARASIL

    齋藤 理恵, 小野寺 理, 柿田 明美

    Clinical Neuroscience   40 ( 6 )   700 - 702   2022.6

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    Language：Japanese   Publisher：(株)中外医学社  

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  • 臨床医のための神経病理再入門 小脳・脳幹梗塞

    佐藤 朋江, 齊ノ内 信, 齋藤 理恵, 柿田 明美

    Clinical Neuroscience   40 ( 2 )   148 - 150   2022.2

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    Language：Japanese   Publisher：(株)中外医学社  

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  • 髄膜腫摘出術の7年後に発生した局所浸潤性・再発性fibromatosisの一例

    温 城太郎, 清水 宏, 齋藤 理恵, 渋谷 航平, 棗田 学, 平石 哲也, 佐野 正和, 梅津 哉, 藤井 幸彦, 柿田 明美

    Brain Tumor Pathology   38 ( Suppl. )   121 - 121   2021.5

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    Language：Japanese   Publisher：日本脳腫瘍病理学会  

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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

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  • The diagnosis and management of monogenic cerebral small vessel diseases: Practical guideline by European Academy of Neurology. International journal

    Rie Saito, Vasileios-Arsenios Lioutas

    European journal of neurology   2020.3

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    Language：English  

    Cerebral small vessel disease (cSVD) is a leading cause of stroke and lies at the heart of vascular contributions to dementia. Sporadic cSVD is well-recognized and widely studied, whereas monogenic cSVD is incompletely characterized and understood.

    DOI： 10.1111/ene.14222

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  • 外科的介入を受けていない症候性もやもや病の1剖検例

    齋藤 祥二, 齋藤 理恵, 中原 亜紗, 長谷川 仁, 田口 貴博, 上村 昌寛, 本多 忠幸, 伊藤 靖, 小野寺 理, 梅津 哉, 藤井 幸彦, 柿田 明美

    新潟医学会雑誌   133 ( 11-12 )   389 - 389   2019.12

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  • 神経病理―変性疾患のみかた― αシヌクレイノパチー(2) 多系統萎縮症 Invited

    齋藤 理恵

    病理と臨床   37 ( 7 )   640 - 645   2019.7

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  • 【神経病理update】 遺伝性脳小血管障害の神経病理

    齋藤 理恵, 伊藤 慎治, 野崎 洋明, 柿田 明美

    神経内科   88 ( 5 )   516 - 523   2018.5

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    Language：Japanese   Publisher：(有)科学評論社  

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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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    Language：Japanese   Publisher：信州医学会  

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  • 髄膜播種をきたしたEpithelioid glioblastomaの1例

    金丸 優, 棗田 学, 齋藤 理恵, 野澤 孝徳, 阿部 英明, 岡本 浩一郎, 大石 誠, 藤井 幸彦, 柿田 明美, 信澤 純人

    信州医学雑誌   66 ( 1 )   104 - 105   2018.2

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    Language：Japanese   Publisher：信州医学会  

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  • CADASIL姉弟剖検例の臨床病理所見

    齋藤 理恵, 豊島 靖子, 鈴木 正博, 田中 政春, 野崎 洋明, 小野寺 理, 高橋 均, 柿田 明美

    新潟医学会雑誌   131 ( 5 )   313 - 314   2017.5

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  • PXA with anaplastic features with sarcomatous componentと組織診断した前頭葉腫瘍の1例

    小倉 良介, 伊藤 絢子, 塚本 佳広, 五十川 瑞穂, 齋藤 理恵, 青木 洋, 岡本 浩一郎, 藤井 幸彦, 高橋 均, 柿田 明美

    The Kitakanto Medical Journal   66 ( 2 )   172 - 173   2016.5

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    Language：Japanese   Publisher：北関東医学会  

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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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    Language：Japanese   Publisher：信州医学会  

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  • A case of 77-year-old male with spinocerebellar ataxia type 31 with left dominant dystonia

    Rie Saito, Mami Kanzaki, Yoshikazu Uesaka

    Clinical Neurology   55 ( 6 )   434   2015

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    Language：Japanese   Publishing type：Rapid communication, short report, research note, etc. (scientific journal)   Publisher：Societas Neurologica Japonica  

    DOI： 10.5692/clinicalneurol.cn-000677

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  • 左右差の強い下肢ジストニアをみとめたspinocerebellar ataxia type 31(SCA31)の1例

    齋藤 理恵, 菊野 庄太, 前田 明子, 上坂 義和, 井田 雅祥

    臨床神経学   54 ( 8 )   643 - 647   2014.8

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

    症例は77歳男性である。56歳頃から左下肢の引きずりと、構音障害が出現した。症状は緩徐に進行し発症7年で杖歩行、10年で車いすが必要になった。62歳時当院初診、脊髄小脳変性症の診断にて、タルチレリンを開始した。今回、脳梗塞のため入院した。入院時神経学的所見として右不全片麻痺と小脳失調症状に加え左下肢のジストニアをみとめた。遺伝子検査をおこなったところspinocerebellar ataxia type 31(SCA31)に特異性の高い、PLEKHG4遺伝子の1塩基置換(-16C&gt;T)と、SCA31 locusにおいて挿入変異をみとめSCA31と診断した。ジストニアを呈するSCA31の既報告はなく、貴重な症例と考え報告する。(著者抄録)

    DOI： 10.5692/clinicalneurol.54.643

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  • 左右差の強い下肢ジストニアを認めSCA31が疑われた77歳男性例 Reviewed

    齋藤 理恵, 菊野 庄太, 前田 明子, 上坂 義和, 井田 雅祥

    臨床神経学   53 ( 6 )   488 - 488   2013.6

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

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  • もやもや病を合併したTurner症候群の41歳女性例 Reviewed

    齋藤 理恵, 吉田 達彌, 堤内 路子, 前田 明子, 上坂 義和, 原 貴行

    臨床神経学   53 ( 2 )   144 - 144   2013.2

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

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  • IVt-PA例と血管内治療追加例の検討 Reviewed

    齋藤 理恵, 堤内 路子, 前田 明子, 上坂 義和, 早川 幹人, 松丸 祐司

    臨床神経学   52 ( 12 )   1420 - 1420   2012.12

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

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  • ステロイド治療にて低左心機能、アミオダロン誘発性甲状腺中毒症を救命しえた1例

    齋藤 理恵, 三谷 治夫, 田尾 進, 石綿 清雄, 山口 徹, 大野 実, 竹内 靖博

    日本内科学会雑誌   98 ( 10 )   2589 - 2591   2009.10

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    Language：Japanese   Publisher：(一社)日本内科学会  

    72歳男。患者は体重減少、全身倦怠感を主訴とした。拡張型心筋症で両心室ペーシングを挿入しており、2005年に発作性心房細動に対してアミオダロンを導入した。しかし、2008年2月から徐々にF-T4の上昇とTSH(thyroid stimulating hormone)の低下がみられ、同年6月の外来で明らかな甲状腺中毒症を認め、精査加療のため入院となった。甲状腺99mTcシンチグラムでは甲状腺機能亢進症は否定的で、アミオダロン内服によってII型のamiodarone-induced-thyrotoxicosis(AIT)、破壊性甲状腺炎型が生じたものと考えられた。そこで、アミオダロンを中止して10日間経過をみたが、甲状腺ホルモンの有意な低下を認めず、プレドニゾロン30mgの内服を開始した。開始後2週間目にはF-T3が正常化し、臨床的にも改善が認められ、更に2ヵ月後にはF-T4が、3ヵ月後にはTSHも正常化した。以上、AITでは早期のもT3低下作用を期待して、ステロイド治療を検討すべきと考えられた。

    DOI： 10.2169/naika.98.2589

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    Other Link： https://jlc.jst.go.jp/DN/JALC/00338907156?from=CiNii

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Presentations

  • 脳血管障害の病理 -脳梗塞と脳出血を中心に- Invited

    齋藤理恵

    日本病理学会診断病理サマーフェスト  2023.9 

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    Presentation type：Public lecture, seminar, tutorial, course, or other speech  

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  • HTRA1-related small vessel disease: vascular degeneration revealed by 3D pathologic analysis and fibulin5 immunostaining

    R Saito, T Kato, M Uemura, Y Saito, S Murayama, K Tainaka, O Onodera, A Kakita

    American Association of Neuropathologists  2023.6 

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    Presentation type：Poster presentation  

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  • Gordon Holmes syndrome and SCA17-DI: pathology of 2 unrelated patients with Huntington-like disorder

    Rie Saito, Yui Tada, Daisuke Oikawa, Yusuke Sato, Keisuke Iwanaga, Akira Satoh, Makiko Seto, Kodai Kume, Nozomi Ueki, Masahiro Nakashima, Shintaro Hayashi, Yasuko Toyoshima, Fuminori Tokunaga, Hideshi Kawakami, Akiyoshi Kakita

    The 64rd annual meeting of the Japanese Society of Neuropathology  2023.6 

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    Presentation type：Oral presentation (general)  

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  • Pathologic analysis for a better understanding of the pathophysiology of small vessel diseases

    2023.5 

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    Presentation type：Symposium, workshop panel (public)  

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  • 脳血管障害 Invited

    齋藤理恵

    2022.6 

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    Presentation type：Public lecture, seminar, tutorial, course, or other speech  

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  • Fibrin5 immunoprofiles in terms of diagnosis of HTRA1-related small vessel disease

    2022.6 

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    Presentation type：Oral presentation (general)  

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  • 脊髄小脳変性症：見てみよう神経病理 Invited

    齋藤理恵

    神経学会学術集会  2022.5 

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    Presentation type：Public lecture, seminar, tutorial, course, or other speech  

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  • Cerebral small vessel disease: white matter degeneration revealed by 3D histopathologic evaluation

    Rie Saito

    The 62nd annual meeting of the Japanese Society of Neuropathology  2021.5 

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  • 3D histopathologic analysis of degenerative vasculature and white matte in small-vessel diseases

    Rie Saito, Akiyoshi Kakita

    The 10thNIPS-PRI-BRINU. joint Symposium  2021.3 

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  • 孤発性脳小血管病とCADASIL：剖検脳の白質変性に関する組織像の定量的解析

    齋藤 理恵

    第60回神経病理学会総会  2019.7 

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  • Small vessel characteristics of autopsied patients with CADASIL and those heterozygous for HTRA1 mutations: 3D analysis using the Cubic tissue clearing technique

    Rie Saito, Kazuki Tainaka, Akiyoshi Kakita

    American Academy of Neurology, 2019 annual meeting  2019.5 

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  • CADASIL and CARASIL Invited International conference

    齋藤 理恵

    19th International Congress of Neuropathology  2018.9 

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

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Awards

  • Excellent English oral presentation Award

    2021.5   Japanese society of Neuropathology   cerebral small vessel disease: white matter degeneration revealed by 3D histopathologic evaluation

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  • 第57回神経病理学会総会学術研究会 優秀ポスター賞

    2016.6   日本神経病理学会  

    齋藤 理恵

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Research Projects

  • 脳小血管の細胞外基質の摂動を起こす細胞群の同定と、その制御機構の解読

    Grant number：22H00466

    2022.4 - 2025.3

    System name：科学研究費助成事業

    Research category：基盤研究(A)

    Awarding organization：日本学術振興会

    小野寺 理, 加藤 泰介, 塚田 啓道, 齋藤 理恵

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    Grant amount：\42510000 （ Direct Cost: \32700000 、 Indirect Cost：\9810000 ）

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  • Cerebral microangiopathy: To clarify the pathologic basis and pathomechanism

    Grant number：20K16595

    2020.4 - 2024.3

    System name：Grants-in-Aid for Scientific Research Grant-in-Aid for Early-Career Scientists

    Research category：Grant-in-Aid for Early-Career Scientists

    Awarding organization：Japan Society for the Promotion of Science

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    Grant amount：\4160000 （ Direct Cost: \3200000 、 Indirect Cost：\960000 ）

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  • Development of "3D Digital Neuropathology" as a new academic field

    Grant number：20K20468

    2019.6 - 2022.3

    System name：Grants-in-Aid for Scientific Research Grant-in-Aid for Challenging Research (Pioneering)

    Research category：Grant-in-Aid for Challenging Research (Pioneering)

    Awarding organization：Japan Society for the Promotion of Science

    Kakita Akiyoshi

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    Grant amount：\25870000 （ Direct Cost: \19900000 、 Indirect Cost：\5970000 ）

    The brain is a complex structure, and its functional units are especially three-dimensional. In this study, we developed a technological platform to capture the arrangement and network of neurons and glial cells, as well as the distribution of microvessels, in three dimensions by using transparency of human brain tissue and 3D imaging technology. First, we overcame the biggest optical challenges in human brain tissue, autofluorescence and browning, and succeeded in developing transparency reagents specifically for human brain tissue. Next, we established various general fluorescent staining and whole-mount immunostaining techniques for 3D. As a result, we have established an imaging platform for whole-mount visualization of many types of structures, including neurons, glial cells, microvessels, myelin sheaths, and senile plaques.

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  • 血管性認知症：脳小血管病の臨床病理診断基準の確立へ向けて

    2018.8 - 2020.3

    System name：科学研究費：研究活動スタート支援

    Awarding organization：日本学術振興会

    齋藤 理恵

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    Authorship：Principal investigator  Grant type：Competitive

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Other research activities