研究者詳細 - 小野寺　理

論文 - 小野寺　理

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Atrophy of the cerebellum and brainstem in dentatorubral pallidoluysian atrophy - Influence of CAG repeat size on MRI findings 査読

R Koide, O Onodera, T Ikeuchi, R Kondo, H Tanaka, S Tokiguchi, A Tomoda, T Miike, F Isa, H Beppu, N Shimizu, Y Watanabe, Y Horikawa, T Shimohata, K Hirota, A Ishikawa, S Tsuji

NEUROLOGY 49 ( 6 ) 1605 - 1612 1997年12月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：LIPPINCOTT WILLIAMS & WILKINS

To elucidate how the size of the expanded CAG repeat of the gene for dentatorubral pallidoluysian atrophy (DRPLA) and other factors affect the atrophy of the brainstem and cerebellum, and the appearance of high-intensity signals on T2-weighted MRI of the cerebral white matter of patients with DRPLA, we quantitatively analyzed the MRI findings of 26 patients with DRPLA, the diagnosis of which was confirmed by molecular analysis of the DRPLA gene. When we classified the patients into two groups based on the size of the expanded CAG repeat of the DRPLA gene (group 1, number of CAG repeat units greater than or equal to 66; group 2, number of CAG repeat units less than or equal to 65), we found strong inverse correlations between the age at MRI and the areas of midsagittal structures of the cerebellum and brainstem in group 1 but not in group 2. Multiple regression analysis, however, revealed that both the patient's age at MRI and the size of the expanded CAG repeat correlated with the areas of midsagittal structures. Involvement of the cerebral white matter as detected on T2-weighted images was observed more frequently in patients belonging to group 2 than in group 1 patients. Furthermore it was demonstrated that high-intensity signals can be detected on T2-weighted images of the cerebral white matter of patients with a largely expanded CAG repeat (group I) in their thirties. These results suggest that patient age as well as the size of the expanded CAG repeat are related to the degree of atrophy of the brainstem and cerebellum, and the white matter changes in patients with DRPLA.

Transglutaminase-catalyzed inactivation of glyceraldehyde 3-phosphate dehydrogenase and alpha-ketoglutarate dehydrogenase complex by polyglutamine domains of pathological length 査読

AJL Cooper, KFR Sheu, Burke, JR, O Onodera, WJ Stritmatter, AD Roses, JP Blass

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA 94 ( 23 ) 12604 - 12609 1997年11月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：NATL ACAD SCIENCES

Several adult-onset neurodegenerative diseases are caused by genes with expanded CAG triplet repeats within their coding regions and extended polyglutamine (a) domains within the expressed proteins. Generally, in clinically affected individuals n greater than or equal to 40. Glyceraldehyde 3-phosphate dehydrogenase binds tightly to four Q(n) disease proteins, but the significance of this interaction is unknown. We now report that purified glyceraldehyde 3-phosphate dehydrogenase is inactivated by tissue transglutaminase in the presence of glutathione S-transferase constructs containing a a domain of pathological length (n = 62 or 81). The dehydrogenase is less strongly inhibited by tissue transglutaminase in the presence of constructs containing shorter Q(n) domains (n = 0 or 10). Purified cr-ketoglutarate dehydrogenase complex also is inactivated by tissue transglutaminase plus glutathione S-transferase constructs containing pathological-length a domains (n = 62 or 81). The results suggest that tissue transglutaminase-catalyzed covalent linkages involving the larger poly-Q domains may disrupt cerebral energy metabolism in CAG/Q(n) expansion diseases.

DOI： 10.1073/pnas.94.23.12604

Oligomerization of expanded-polyglutamine domain fluorescent fusion proteins in cultured mammalian cells 査読

O Onodera, Burke, JR, SE Miller, S Hester, S Tsuji, AD Roses, WJ Strittmatter

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 238 ( 2 ) 599 - 605 1997年9月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS

Six inherited neurologic diseases, including Huntington's disease, result from the expansion of a CAG domain of the disease genes to produce a domain of more than 40 glutamines in the expressed protein. The mechanism by which expansion of this polyglutamine domain causes disease is unknown. Recent studies demonstrated oligomerization of polyglutamine-domain proteins in mammalian neurons. To study oligomerization of polyglutamine proteins and to identify heterologous protein interactions, varying length polyglutamine-green fluorescent protein fusion proteins were expressed in cultured COS-7 cells. The 19- and 35-glutamine fusion proteins (non-pathologic length) distributed diffusely throughout the cytoplasm. In contrast, 56- and 80-glutamine fusion proteins (pathologic length) formed fibrillar arrays resembling those previously observed in neurons in Huntington's disease and in a transgenic mouse model. These aggregates were intranuclear and intracytoplasmic. Intracytoplasmic aggregates were surrounded by collapsed intermediate filaments, The intermediate filament protein vimentin co-immunoisolated with expanded polyglutamine fusion proteins. This cellular model will expedite investigations into oligomerization of polyglutamine proteins and their interactions with other proteins. (C) 1997 Academic Press.

DOI： 10.1006/bbrc.1997.7337

Polyglutamine domains are substrates of tissue transglutaminase: Does transglutaminase play a role in expanded CAG/poly-Q neurodegenerative diseases? 査読

AJL Cooper, KFR Sheu, Burke, JR, O Onodera, WJ Strittmatter, AD Roses, JP Blass

JOURNAL OF NEUROCHEMISTRY 69 ( 1 ) 431 - 434 1997年7月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：LIPPINCOTT-RAVEN PUBL

Huntington's disease and six other neurodegenerative diseases are associated with abnormal gene products containing expanded polyglutamine (poly-Q; Q(n)) domains (n > 40). in the present work, we show that glutathione S-transferase (GST) fusion proteins containing a small, physiological-length poly-Q domain (GSTQ(10)) or a large, pathological-length poly-Q domain (GSTQ(62)) are excellent substrates of guinea pig liver (tissue) transglutaminase and that both GSTQ(10) and GSTQ(62) are activators of tissue transglutaminase-catalyzed hydroxaminolysis of N-alpha-carbobenzoxyglutaminylglycine. The present findings have implications for understanding the pathophysiological mechanisms of expanded CAG/poly-Q domain diseases.

DOI： 10.1046/j.1471-4159.1997.69010431.x

Molecular cloning of murine homologue dentatorubral-pallidoluysian atrophy (DRPLA) cDNA: Strong conservation of a polymorphic CAG repeat in the murine gene 査読

M Oyake, O Onodera, T Shiroishi, H Takano, Y Takahashi, R Kominami, K Moriwaki, T Ikeuchi, S Igarashi, H Tanaka, S Tsuji

GENOMICS 40 ( 1 ) 205 - 207 1997年2月

Changes in anti-HuD antibody titers in the long-term course in paraneoplastic sensory neuropathy 査読

Y Yagi, T Inuzuka, K Takada, R Nakano, Hozumi, I, H Yoshimoto, O Onodera, K Tanaka, S Sato, M Takahashi

EUROPEAN NEUROLOGY 37 ( 2 ) 122 - 123 1997年

Toxicity of expanded polyglutamine-domain proteins in Escherichia coli 査読

O Onodera, AD Roses, S Tsuji, JM Vance, WJ Strittmatter, Burke, JR

FEBS LETTERS 399 ( 1-2 ) 135 - 139 1996年12月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：ELSEVIER SCIENCE BV

Five neurodegenerative diseases are caused by proteins with expanded polyglutamine domains. Toxicity of these proteins has been previously identified only in mammals, and no simple model systems are available. In this paper, we demonstrate in E. coli that long polyglutamine domains (59-81 residues) as GST-fusion proteins inhibit growth while smaller glutamine (10-35 residues) or polyalanine (61 residues) domains have no effect. Analogously in humans, polyglutamine repeats less than 35-40 glutamines produce a normal phenotype, while expansion greater than 40 glutamines is always associated with disease. Expression of polyglutamine proteins in E. coli may help identify the molecular mechanism of pathogenesis of CAG trinucleotide repeat diseases and be a useful screen to identify potential therapeutic compounds.

DOI： 10.1016/S0014-5793(96)01301-4

Lack of association of very low density lipoprotein receptor gene polymorphism with Caucasian Alzheimer's disease 査読

K Okuizumi, O Onodera, K Seki, H Tanaka, Y Namba, K Ikeda, AM Saunders, MA PericakVance, AD Roses, S Tsuji

ANNALS OF NEUROLOGY 40 ( 2 ) 251 - 254 1996年8月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：LITTLE BROWN CO

To determine whether the association of the very low density lipoprotein receptor (VLDL-R) gene with Alzheimer's disease (AD), which has recently been identified in Japanese AD patients, is commonly observed in AD patients of other ethnic backgrounds, we have investigated the allele frequency of the polymorphic CGG repeat in the 5'-UTR of the VLDL-R gene using a data set of 84 caucasian AD patients with 104 caucasian controls. Although the allele frequency of the 8-repeat allele was slightly lower, and that of 9-repeat allele was slightly higher, in the caucasian AD patients than in caucasian controls, the differences were not statistically significant. Multiple logistic regression analysis using apolipoprotein E4 (APOE4) allele, 5-, 8-, or 9-repeat allele of the VLDL-R gene, sex, and age at onset as the predictors revealed that only the APOE4 allele was significantly associated with AD in the data set of the caucasian AD patients and controls.

DOI： 10.1002/ana.410400220

Association study between schizophrenia and dopamine D3 receptor gene polymorphism 査読

T Tanaka, S Igarashi, O Onodera, H Tanaka, M Takahashi, M Maeda, K Kameda, S Tsuji, S Ihda

AMERICAN JOURNAL OF MEDICAL GENETICS 67 ( 4 ) 366 - 368 1996年7月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：WILEY-LISS

Crocq et al, [1992: J Med Genet 29:858-860] reported the existence of an association between schizophrenia and homozygosity of a Ball polymorphism in the first exon of the dopamine D3 receptor (DRD3) gene, In response to this report, further studies were conducted; however, these studies yielded conflicting results, In the present study, we examined 100 unrelated Japanese schizophrenics and 100 normal controls to determine any association between this polymorphism and schizophrenia, Results suggest that neither allele nor genotype frequencies of the DRD3 gene in the schizophrenics as a whole are significantly different from those of the controls, Further, we found no association between any allele or genotype and any clinical subtype based on family history of schizophrenia and age-at-onset, A significantly high frequency of homozygosity of a dopamine D3 receptor gene allele was not observed in the schizophrenics as a whole, or in clinical subtypes, Our results suggest that an association between the dopamine D3 receptor gene and schizophrenia is unlikely to exist. (C) 1996 Wiley-Liss, Inc.

DOI： 10.1002/(SICI)1096-8628(19960726)67:4<366::AID-AJMG9>3.0.CO;2-K

Non-Mendelian transmission in Dentatorubral-Pallidoluysian atrophy and Machado-Joseph disease: The mutant allele is preferentially transmitted in male meiosis 査読

T Ikeuchi, S Igarashi, Y Takiyama, O Onodera, M Oyake, H Takano, R Koide, H Tanaka, S Tsuji

AMERICAN JOURNAL OF HUMAN GENETICS 58 ( 4 ) 730 - 733 1996年4月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：UNIV CHICAGO PRESS

Autosomal dominant dentatorubral-pallidoluysian atrophy (DRPLA) and Machado-Joseph disease (MJD) are neurodegenerative disorders caused by CAG trinucleotide repeat expansions. An inverse correlation of age at onset with the length of the expanded CAG trinucleotide repeats has been demonstrated, and the intergenerational instability of the length of the CAG trinucleotide repeats, which is more prominent in paternal than in maternal transmissions, has been shown to underlie the basic mechanisms of anticipation in DRPLA and MJD. Our previous observations on DRPLA and MJD pedigrees, as well as a review of the literature, have suggested that the numbers of affected offspring exceed those of unaffected offspring, which is difficult to explain by the Mendelian principle of random segregation of alleles. In the present study, we analyzed the segregation patterns in 211 transmissions in 24 DRPLA pedigrees and 80 transmissions in 7 MJD pedigrees, with the diagnoses confirmed by molecular testing. Significant distortions in favor of transmission of the mutant alleles were found in male meiosis, where the mutant alleles were transmitted to 62% of all offspring in DRPLA (chi(2) = 7.69; P < .01) and 73% in MJD (chi(2) = 6.82; P < .01). The results were consistent with meiotic drive in DRPLA and MJD. Since more prominent meiotic instability of the length of the CAG trinucleotide repeats is observed in male meiosis than in female meiosis and meiotic drive is observed only in male meiosis, these results raise the possibility that a common molecular mechanism underlies the meiotic drive and the meiotic instability in male meiosis.

Lack of association between dopamine D2 receptor gene Cys311 variant and schizophrenia 査読

T Tanaka, S Igarashi, O Onodera, H Tanaka, N Fukushima, M Takahashi, K Kameda, S Tsuji, S Ihda

AMERICAN JOURNAL OF MEDICAL GENETICS 67 ( 2 ) 208 - 211 1996年4月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：WILEY-LISS

Itokawa et al, [1993] reported identifying one missense nucleotide mutation from C to G resulting in a substitution of serine with cysteine at codon 311 in the third intracellular loop of the dopamine D2 receptor in schizophrenics, Arinami et al, [1994] reported finding a positive association between the Cys311 variant and schizophrenia. In response to the report by Arinami et al, [1994] we examined 106 unrelated Japanese schizophrenics and 106 normal controls to determine if there is any association of the Cys311 variant with schizophrenia. However, we found no statistically significant differences in allelic frequencies of Cys311 between schizophrenia and normal controls. The present results as well as those of all previous studies except for that of Arinami et al. [1994] indicated that an association between the dopamine D2 receptor gene and schizophrenia is unlikely to exist. (C) 1996 Wiley-Liss, Inc.

DOI： 10.1002/(SICI)1096-8628(19960409)67:2<208::AID-AJMG12>3.0.CO;2-N

Somatic mosaicism of CAG repeat expansion could be associated with brain shrinkage in DRPLA

Takano, H., Onodera, O., Takahashi, H., Yamada, M., Igarashi, S., Oyakei, M., Ikeuchii, T., Koide, R., Tanaka, H., Iwabuchi, K., Tsuji, S.

Japanese Journal of Human Genetics 41 ( 1 ) 33 - 33 1996年

Molecular cloning of murine homologue cdna for dentatorubral-pallidoluysian atrophy (DRPLA) gene

Oyake, M., Onodera, O., Shiroishi, T., Takano, H., Igarashi, S., Tanaka, H., Moriwaki, K., Tsuji, S.

Japanese Journal of Human Genetics 41 ( 1 ) 91 - 91 1996年

Lack of association between dopamine D4 receptor gene and schizophrenia 査読

T Tanaka, S Igarashi, O Onodera, H Tanaka, K Kameda, K Takahashi, S Tsuji, S Ihda

AMERICAN JOURNAL OF MEDICAL GENETICS 60 ( 6 ) 580 - 582 1995年12月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：WILEY-LISS

An intriguing property of the dopamine D4 receptor gene is a hypervariable segment in the coding region characterized by a varying number of direct imperfect 48 bp repeats (2-8 or 10 repeats) in the third exon of he gene [Lichter et al., 1993: Hum Mol Genet 2:767-773]. The authors analyzed 70 unrelated schizophrenics and 70 normal controls to determine the allele and genotype frequencies created by length polymorphism of dopamine D4 receptor gene. All patients and controls were unrelated and from the Japanese population. Patients were divided into three groups with regard to age at onset, familial loading, and severity of symptoms assessed strictly with Manchester scale. There were no statistically significant differences if the distributions of alleles and genotypes were analyzed for schizophrenia as a whole or analyzed in consideration of those clinical subtypes, Lichter and colleagues [1993] have reported that at least 25 haplotypes exist for this polymorphic region of the. dopamine receptor D4 gene, In this study only the alleles created by length polymorphism were analyzed, and further investigation to determine the haplotypes of patients and controls on using a much larger sample size will be required. (C) 1995 Wiley-Liss, Inc.

DOI： 10.1002/ajmg.1320600620

DENTATORUBRAL-PALLIDOLUYSIAN ATROPHY - CLINICAL-FEATURES ARE CLOSELY-RELATED TO UNSTABLE EXPANSIONS OF TRINUCLEOTIDE (CAG) REPEAT 査読

T IKEUCHI, R KOIDE, H TANAKA, O ONODERA, S IGARASHI, H TAKAHASHI, R KONDO, A ISHIKAWA, A TOMODA, T MIIKE, K SATO, Y IHARA, T HAYABARA, F ISA, H TANABE, S TOKIGUCHI, M HAYASHI, N SHIMIZU, F IKUTA, H NAITO, S TSUJI

ANNALS OF NEUROLOGY 37 ( 6 ) 769 - 775 1995年6月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：LITTLE BROWN CO

Dentatorubral-pallidoluysian atrophy is an autosomal dominant neurodegenerative disease characterized by various combinations of ataxia, choreoathetosis, myoclonus, epilepsy, and dementia as well as a wide range of ages at onset. A specific unstable trinucleotide repeat expansion in a gene on the short arm of chromosome 12 was recently identified as the pathogenic mutation for this disease. We investigated how the degree of expansion of the CAG repeat affects the clinical manifestations of dentatorubral-pallidoluysian atrophy. The size of the expanded alleles was well correlated with the age at onset (r = -0.696, p < 0.001). Patients with the progressive myoclonus epilepsy phenotype had larger expansions (62-79 repeats) and an earlier age at onset (onset before age 21). Furthermore, most of the patients with the progressive myoclonus epilepsy phenotype inherited their expanded alleles from their affected fathers. On the other hand, patients with the non-progressive myoclonus epilepsy phenotype showed smaller expansions (54-67 repeats) and a later age at onset (onset at or after age 21). Detailed analyses of clinical features demonstrated that ataxia, involuntary movement of either myoclonus or choreoathetosis, and intellectual decline are cardinal features of dentatorubral-pallidoluysian atrophy, with myoclonus and epilepsy being observed more frequently in patients with an earlier age at onset. Thus the wide variation in clinical manifestations of dentatorubral-pallidoluysian atrophy can now be clearly explained based on the degree of CAG repeat expansion, which strongly indicates that the expanded alleles are intimately involved in the neuronal degeneration in dentatofugal and pallidofugal systems.

DOI： 10.1002/ana.410370610

TRIAL TO ESTABLISH AN ANIMAL-MODEL OF PARANEOPLASTIC CEREBELLAR DEGENERATION WITH ANTI-YO ANTIBODY .1. MOUSE STRAINS BEARING DIFFERENT MHC MOLECULES PRODUCE ANTIBODIES ON IMMUNIZATION WITH RECOMBINANT YO PROTEIN, BUT DO NOT CAUSE PURKINJE-CELL LOSS 査読

M TANAKA, K TANAKA, O ONODERA, S TSUJI

CLINICAL NEUROLOGY AND NEUROSURGERY 97 ( 1 ) 95 - 100 1995年2月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：VAN GORCUM CO BV

Passive transfer of anti-Yo antibody from patients with paraneoplastic cerebellar degeneration (PCD) associated with gynecological or breast carcinoma has not been successful in inducing an animal model. We used active immunization with recombinant Yo protein of four strains of mice bearing different MHC molecules: BALB/c (H-2d), C3H (H-2k), C57BL/6 (H-2b), SJL/J (H-2s). All the strains produced high anti-Yo antibody titer but none developed cerebellar ataxia or showed Purkinje cell loss. Spleen cells from the immunized mice also reacted with recombinant protein. Because C57BL/6(nu/nu) mice produce no anti-Yo antibody, mature helper T cells are required for its production. Results suggest that antibody production in peripheral blood alone is not sufficient for the development of PCD and that MHC class II molecules function in the activation of T cells to help B cells produce antibodies.

LONG-TERM COURSE OF CHANGE IN ANTI-YO ANTIBODY CONTENT IN PARANEOPLASTIC CEREBELLAR DEGENERATION 査読

K TANAKA, M TANAKA, S IGARASHI, O ONODERA, T NAKAJIMA, M YAMAZAKI, T MIYATAKE, S TSUJI

JOURNAL OF NEUROLOGY NEUROSURGERY AND PSYCHIATRY 58 ( 2 ) 256 - 257 1995年2月

DENTATORUBRAL-PALLIDOLUYSIAN ATROPHY (DRPLA) - CLOSE CORRELATION OF CAG REPEAT EXPANSIONS WITH THE WIDE SPECTRUM OF CLINICAL PRESENTATIONS AND PROMINENT ANTICIPATION 査読

T IKEUCHI, O ONODERA, M OYAKE, R KOIDE, H TANAKA, S TSUJI

SEMINARS IN CELL BIOLOGY 6 ( 1 ) 37 - 44 1995年2月

記述言語：英語出版者・発行元：ACADEMIC PRESS (LONDON) LTD

Dentatorubral-pallidoluysian atrophy (DRPLA) is a rare autosomal dominant neurodegenerative disease characterized by various combinations of ataxia, choreoathetosis, myoclonus, epilepsy and dementia as well as various ages of onset. We have identified a specific unstable trinucleotide repeat expansion in a gene on the short arm of chromosome 12 as the pathogenic mutation for DRPLA. We investigated how the degree of the expansion of the CAG repeat affects the clinical manifestations of DRPLA. The sires of the expanded alleles were well correlated with the ages of onset (r = -0.6955, P<0.001). Patients with progressive myoclonus epilepsy (PME) phenotype had larger expansions (62-79 repeats) and earlier ages of onset (onset before age 20). Furthermore, most of the patients with PME phenotype inherited their expanded alleles from their affected fathers. On the other hand, patients with non-PME phenotype showed later ages of onset (onset after age 20) and smaller expansions (54-67 repeats). When ages of onset of each clinical symptom are compared with sizes of the CAG repeat, there is again a remarkably high correlation of the sizes of CAG repeat with each of the clinical symptoms. Thus the wide variation in clinical manifestations of DRPLA can now be clearly explained based on-the degree of CAG repeat expansion, which strongly indicates that the expanded alleles are intimately involved in the neuronal degeneration in dentatofugal and pallidofugal systems.

TRIAL TO ESTABLISH AN ANIMAL-MODEL OF PARANEOPLASTIC CEREBELLAR DEGENERATION WITH ANTI-YO ANTIBODY .2. PASSIVE TRANSFER OF MURINE MONONUCLEAR-CELLS ACTIVATED WITH RECOMBINANT YO PROTEIN TO PARANEOPLASTIC CEREBELLAR DEGENERATION LYMPHOCYTES IN SEVERE COMBINED IMMUNODEFICIENCY MICE 査読

K TANAKA, M TANAKA, S IGARASHI, O ONODERA, T MIYATAKE, S TSUJI

CLINICAL NEUROLOGY AND NEUROSURGERY 97 ( 1 ) 101 - 105 1995年2月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：VAN GORCUM CO BV

Passive transfer of serum IgG or mononuclear cells from peripheral blood of a patient with paraneoplastic cerebellar degeneration (PCD) to rodents was carried out in order to examine the role of anti-Purkinje cell antibody (anti-Yo antibody) present in serum and cerebrospinal fluid of PCD patients. After a single injection of IgG into mouse brain, it was taken up by Purkinje cells and remained there for more than 36 h without Purkinje cell loss. Injection of PCD IgG together with complement or lipopolysaccharide-activated human macrophages or rat mononuclear cells into rat ventricles did not cause Purkinje cell loss. We also studied passive transfer of the PCD patient's lymphocytes to mice with severe combined immunodeficiency (SCID). We constructed a recombinant Yo fusion protein that has the leucine-zipper protein (Yo protein), the common epitope for anti-Yo antibody for immunizing mice, and that resulted in production of significant amounts of anti-Yo antibody. Spleen cells from these Yo protein immunized mice were injected intravenously or intracerebrally into naive mice that subsequently showed no neurological symptoms or loss of Purkinje cells. We conclude that the anti-Yo antibody, either in combination with or without complement or activated mononuclear cells, cannot be the sole cause of Purkinje cell loss.

Auditory comprehension in transcortical motor aphasia due to a medial lesions of the left frontal lobe 査読

M. Otsuki, Y. Soma, O. Onodera, S. Tsuji, A. Satoh, N. Yamada

Brain and Nerve 47 ( 11 ) 1081 - 1085 1995年

記述言語：日本語掲載種別：研究論文（学術雑誌）

We assessed the anatomical findings and auditory comprehension of six patients with transcortical motor aphasia due to medial lesions of the left frontal lobe. All patients were right handed and were initially mute for several hours after the onset, and they exhibited mild paresis of the right lower extremity. Their spontaneous speech was sparse and not fluent, and sometimes accompanied by echolalia, but their articulation was normal and repetition was excellent. They had difficulty in recalling words. A diagnosis of transcortical motor aphasia was made on the basis of their clinical symptoms. All patients were found to have an infarct in the left medial frontal region by MRI and/or CT. We administered the Western Aphasia Battery and 50 line drawing pointing task in order to evaluate auditory comprehension. Based on the results we concluded that there is no impairment of auditory comprehension of single words when lesions are limited to the superior frontal gyrus, but that lesions extending to the middle frontal gyrus interfere with auditory comprehension of single words. Our observations indicate that the middle frontal gyrus plays an important role in auditory comprehension of single words. All of the patients displayed impaired auditory comprehension of sentences even when their lesions were strictly limited to the medial frontal lobe. This suggests that the medial frontal lobe plays some role in the auditory comprehension of sentences.

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