2025/07/29 更新

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写真a

ハシグチ　シュンタ
橋口 俊太
Shunta Hashiguchi
所属
医学研究科 医科学専攻 神経内科学・脳卒中医学 助教
医学部 医学科
職名
助教
プロフィール

脊髄小脳変性症のモデルマウスを作成し、パッチクランプ法を用いた電気生理学的アプローチにより病態を解明してきた。

外部リンク

学位

  • 博士（医学） （ 2020年3月   横浜市立大学 ）

研究キーワード

  • 脊髄小脳変性症の病態解明と治療法開発

研究分野

  • ライフサイエンス / 神経内科学

論文

  • Ataxic phenotype with altered CaV3.1 channel property in a mouse model for spinocerebellar ataxia 42. 査読 国際誌

    Shunta Hashiguchi, Hiroshi Doi, Misako Kunii, Yukihiro Nakamura, Misa Shimuta, Etsuko Suzuki, Shigeru Koyano, Masaki Okubo, Hitaru Kishida, Masaaki Shiina, Kazuhiro Ogata, Fumiko Hirashima, Yukichi Inoue, Shun Kubota, Noriko Hayashi, Haruko Nakamura, Keita Takahashi, Atsuko Katsumoto, Mikiko Tada, Kenichi Tanaka, Toshikuni Sasaoka, Satoko Miyatake, Noriko Miyake, Hirotomo Saitsu, Nozomu Sato, Kokoro Ozaki, Kiyobumi Ohta, Takanori Yokota, Hidehiro Mizusawa, Jun Mitsui, Hiroyuki Ishiura, Jun Yoshimura, Shinichi Morishita, Shoji Tsuji, Hideyuki Takeuchi, Kinya Ishikawa, Naomichi Matsumoto, Taro Ishikawa, Fumiaki Tanaka

    Neurobiology of disease   130   104516 - 104516   2019年10月

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    記述言語：英語  

    Spinocerebellar ataxia 42 (SCA42) is a neurodegenerative disorder recently shown to be caused by c.5144G > A (p.Arg1715His) mutation in CACNA1G, which encodes the T-type voltage-gated calcium channel CaV3.1. Here, we describe a large Japanese family with SCA42. Postmortem pathological examination revealed severe cerebellar degeneration with prominent Purkinje cell loss without ubiquitin accumulation in an SCA42 patient. To determine whether this mutation causes ataxic symptoms and neurodegeneration, we generated knock-in mice harboring c.5168G > A (p.Arg1723His) mutation in Cacna1g, corresponding to the mutation identified in the SCA42 family. Both heterozygous and homozygous mutants developed an ataxic phenotype from the age of 11-20 weeks and showed Purkinje cell loss at 50 weeks old. Degenerative change of Purkinje cells and atrophic thinning of the molecular layer were conspicuous in homozygous knock-in mice. Electrophysiological analysis of Purkinje cells using acute cerebellar slices from young mice showed that the point mutation altered the voltage dependence of CaV3.1 channel activation and reduced the rebound action potentials after hyperpolarization, although it did not significantly affect the basic properties of synaptic transmission onto Purkinje cells. Finally, we revealed that the resonance of membrane potential of neurons in the inferior olivary nucleus was decreased in knock-in mice, which indicates that p.Arg1723His CaV3.1 mutation affects climbing fiber signaling to Purkinje cells. Altogether, our study shows not only that a point mutation in CACNA1G causes an ataxic phenotype and Purkinje cell degeneration in a mouse model, but also that the electrophysiological abnormalities at an early stage of SCA42 precede Purkinje cell loss.

    DOI： 10.1016/j.nbd.2019.104516

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  • Siponimod inhibits microglial inflammasome activation. 国際誌

    Hiroyasu Komiya, Hideyuki Takeuchi, Akihiro Ogasawara, Yuki Ogawa, Shun Kubota, Shunta Hashiguchi, Keita Takahashi, Misako Kunii, Kenichi Tanaka, Mikiko Tada, Hiroshi Doi, Fumiaki Tanaka

    Neuroscience research   2025年2月

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    記述言語：英語   掲載種別：研究論文（学術雑誌）  

    Siponimod is the first oral drug approved for active secondary progressive multiple sclerosis. It acts as a functional antagonist of sphingosine-1-phosphate (S1P) receptor 1 (S1P1) through S1P1 internalization, and also serves an agonist of S1P5; however, the detailed mechanisms of its therapeutic effects on glial cells have yet to be elucidated. In this study, we investigated the anti-inflammatory mechanism of siponimod in microglia. Pretreatment with either siponimod or the S1P1 antagonist W146 significantly suppressed the production of interleukin-1β in activated microglia stimulated with lipopolysaccharide plus nigericin, an inflammasome activator. Furthermore, siponimod treatment reduced the protein levels of cleaved caspase-1 and inhibited the formation of aggregates of apoptosis-associated speck-like protein containing a C-terminal caspase recruitment domain (ASC specks) in microglia. Our data indicate that siponimod achieves its anti-inflammatory effects by inhibiting inflammasome activation in microglia via S1P1 antagonism. This process is inferred to play a crucial role in mitigating the secondary progression of multiple sclerosis, where microglial activation in the gray matter is considered a key pathological factor.

    DOI： 10.1016/j.neures.2025.02.002

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  • A case report of an individual with Creutzfeldt-Jakob disease characterized by prolonged isolated thalamic lesions and rare MM2-cortical-type pathology. 国際誌

    Misako Kunii, Hitaru Kishida, Mikiko Tada, Mitsuo Okamoto, Keiichiro Asano, Haruko Nakamura, Keita Takahashi, Shunta Hashiguchi, Shun Kubota, Masaki Okubo, Hideyuki Takeuchi, Naohisa Ueda, Katsuya Satoh, Tetsuyuki Kitamoto, Hiroshi Doi, Fumiaki Tanaka

    BMC neurology   24 ( 1 )   456 - 456   2024年11月

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    記述言語：英語   掲載種別：研究論文（学術雑誌）  

    BACKGROUND: Diffusion-weighted magnetic resonance imaging (DWI) is essential for diagnosing Creutzfeldt-Jakob disease (CJD). Thalamic lesions are rarely detected by DWI in sporadic CJD (sCJD) cases with methionine homozygosity at polymorphic codon 129 (129MM) of the prion protein (PrP) gene. Here, we describe an unusual sCJD case, characterized by prolonged isolated thalamic diffusion hyperintensities and atypical brain pathology, in combination with the 129MM genotype. CASE PRESENTATION: A 72-year-old Japanese man developed a mild unsteady gait that had persisted for 1 year. DWI revealed isolated thalamic diffusion hyperintensities. Over the following 4 years, his condition progressed to include ataxia and cognitive decline. Repeated cerebrospinal fluid tests were negative for 14-3-3 protein, total tau protein, and real-time quaking-induced conversion assay. Electroencephalography did not show periodic sharp wave complexes or generalized periodic discharges. Despite these findings, thalamic DWI abnormalities persisted and evolved to include cortical lesions in the later stage of the disease. Genetic testing confirmed a 129MM genotype with no pathogenic PrP gene variants. Brain autopsy identified type 2 pathogenic PrP and the absence of the M2-thalamic prion strain, suggesting an MM2-cortical (MM2C)-subtype of sCJD. Histopathology revealed small vacuoles (sv) and patchy-perivacuolar PrP deposits without large vacuoles (lv). Patchy-perivacuolar deposits are a characteristic feature of the MM2C (lv) subtype and indicate MM2C (lv) pathology. Thus, this case was classified as a rare MM2C (sv + lv) subtype. No PrP protein staining was observed in the thalamus, despite spongiform changes with small vacuoles. CONCLUSIONS: This case underscores the diagnostic challenges of atypical CJD with isolated thalamic abnormalities on DWI. Despite negative cerebrospinal fluid findings and clinical diagnostic criteria, persistent DWI abnormalities and evolving clinical symptoms continued to raise suspicion of CJD. A definitive diagnosis, being the MM2C (sv + lv) subtype of sCJD, was confirmed upon pathological examination. Even when atypical findings, such as isolated thalamic abnormalities, are observed and various tests are negative, if suspicion of CJD cannot be ruled out, it is important to confirm the diagnosis and pathological subtypes via postmortem analysis.

    DOI： 10.1186/s12883-024-03958-9

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  • UCHL1ヘテロ接合性ナンセンスバリアントを認めた成人発症SPG79の74歳男性例

    豊田 夏実, 古宮 裕泰, 橋口 俊太, 宮地 洋輔, 東山 雄一, 松本 直通, 土井 宏, 田中 章景

    臨床神経学   64 ( 11 )   836 - 836   2024年11月

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    記述言語：日本語   出版者・発行元：(一社)日本神経学会  

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  • Totally Implantable Central Venous Access Port-Associated Bloodstream Infection Caused by Corynebacterium provencense: The First Case Report. 国際誌

    Tetsuta Nishigaki, Katsushi Tanaka, Rika Kawasaki, Shunta Hashiguchi, Hideaki Kato

    Cureus   16 ( 10 )   e71250   2024年10月

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    記述言語：英語   掲載種別：研究論文（学術雑誌）  

    Corynebacterium species are associated with healthcare-associated infections, specifically in device implantation. Here, we report a rare case of a 44-year-old man with a totally implantable central venous access port-related Corynebacterium infection. When he developed a fever on day four of admission, vancomycin treatment was initiated. On the 11th day, the totally implantable central venous access port was removed. Corynebacterium provencense was identified from two sets of blood cultures. Vancomycin treatment was continued for 14 days after port removal, and the patient was discharged home on the 47th day. Although C. provencense infection had not been previously reported in humans, it could be treated by port removal and vancomycin administration, as demonstrated in other reports on Corynebacterium infections.

    DOI： 10.7759/cureus.71250

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  • Lateral olfactory tract usher substance (LOTUS), an endogenous Nogo receptor antagonist, ameliorates disease progression in amyotrophic lateral sclerosis model mice. 国際誌

    Takuya Ikeda, Keita Takahashi, Minatsu Higashi, Hiroyasu Komiya, Tetsuya Asano, Akihiro Ogasawara, Shun Kubota, Shunta Hashiguchi, Misako Kunii, Kenichi Tanaka, Mikiko Tada, Hiroshi Doi, Hideyuki Takeuchi, Kohtaro Takei, Fumiaki Tanaka

    Cell death discovery   9 ( 1 )   454 - 454   2023年12月

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    記述言語：英語   掲載種別：研究論文（学術雑誌）  

    Nogo-Nogo receptor 1 (NgR1) signaling is significantly implicated in neurodegeneration in amyotrophic lateral sclerosis (ALS). We previously showed that lateral olfactory tract usher substance (LOTUS) is an endogenous antagonist of NgR1 that prevents all myelin-associated inhibitors (MAIs), including Nogo, from binding to NgR1. Here we investigated the role of LOTUS in ALS pathogenesis by analyzing G93A-mutated human superoxide dismutase 1 (SOD1) transgenic (Tg) mice, as an ALS model, as well as newly generated LOTUS-overexpressing SOD1 Tg mice. We examined expression profiles of LOTUS and MAIs and compared motor functions and survival periods in these mice. We also investigated motor neuron survival, glial proliferation in the lumbar spinal cord, and neuromuscular junction (NMJ) morphology. We analyzed downstream molecules of NgR1 signaling such as ROCK2, LIMK1, cofilin, and ataxin-2, and also neurotrophins. In addition, we investigated LOTUS protein levels in the ventral horn of ALS patients. We found significantly decreased LOTUS expression in both SOD1 Tg mice and ALS patients. LOTUS overexpression in SOD1 Tg mice increased lifespan and improved motor function, in association with prevention of motor neuron loss, reduced gliosis, increased NMJ innervation, maintenance of cofilin phosphorylation dynamics, decreased levels of ataxin-2, and increased levels of brain-derived neurotrophic factor (BDNF). Reduced LOTUS expression may enhance neurodegeneration in SOD1 Tg mice and ALS patients by activating NgR1 signaling, and in this study LOTUS overexpression significantly ameliorated ALS pathogenesis. LOTUS might serve as a promising therapeutic target for ALS.

    DOI： 10.1038/s41420-023-01758-7

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  • RNA foci in two bi-allelic RFC1 expansion carriers. 国際誌

    Taishi Wada, Hiroshi Doi, Masaki Okubo, Mikiko Tada, Naohisa Ueda, Hidefumi Suzuki, Wakana Tominaga, Haruki Koike, Hiroyasu Komiya, Shun Kubota, Shunta Hashiguchi, Haruko Nakamura, Keita Takahashi, Misako Kunii, Kenichi Tanaka, Yosuke Miyaji, Yuichi Higashiyama, Eriko Koshimizu, Satoko Miyatake, Masahisa Katsuno, Satoshi Fujii, Hidehisa Takahashi, Naomichi Matsumoto, Hideyuki Takeuchi, Fumiaki Tanaka

    Annals of neurology   95 ( 3 )   607 - 613   2023年12月

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    記述言語：英語   掲載種別：研究論文（学術雑誌）  

    Cerebellar ataxia, neuropathy, vestibular areflexia syndrome (CANVAS) is a late-onset, autosomal recessive neurodegenerative disorder caused by biallelic AAGGG/ACAGG repeat expansion (AAGGG-exp/ACAGG-exp) in RFC1. The recent identification of patients with CANVAS exhibiting compound heterozygosity for AAGGG-exp and truncating variants supports the loss-of-function of RFC1 in CANVAS patients. We investigated the pathological changes in two autopsied patients with CANVAS harboring biallelic ACAGG-exp and AAGGG-exp. RNA fluorescence in situ hybridization of the two patients revealed CCTGT- and CCCTT-containing RNA foci, respectively, in neuronal nuclei of tissues with neuronal loss. Our findings suggest that RNA toxicity may be involved in the pathogenesis of CANVAS. This article is protected by copyright. All rights reserved.

    DOI： 10.1002/ana.26848

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  • Anti-inflammatory effects of siponimod on astrocytes. 国際誌

    Akihiro Ogasawara, Hideyuki Takeuchi, Hiroyasu Komiya, Yuki Ogawa, Koki Nishimura, Shun Kubota, Shunta Hashiguchi, Keita Takahashi, Misako Kunii, Kenichi Tanaka, Mikiko Tada, Hiroshi Doi, Fumiaki Tanaka

    Neuroscience research   184   38 - 46   2022年11月

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    記述言語：英語   掲載種別：研究論文（学術雑誌）  

    Siponimod, which is approved to treat active secondary progressive multiple sclerosis, acts as a functional antagonist of sphingosine-1-phosphate (S1P) receptor 1 (S1P1) and an agonist of S1P5. S1P1 antagonization, which inhibits lymphocyte egress from lymphoid tissues and subsequent infiltration into the central nervous system (CNS), is considered the main therapeutic mechanism of siponimod. In addition, siponimod's direct effects on CNS glial cells are another potential neuroprotective mechanism because siponimod can penetrate the blood-brain barrier and CNS glial cells express S1P receptors. However, it remains uncertain whether siponimod directly affects CNS glial cells. In this study, we investigated siponimod's effects on astrocytes using mouse primary cultures. Siponimod suppressed nuclear factor kappa B activation and pro-inflammatory cytokine production. Using antagonists for S1P1 and S1P5, we found that siponimod partially exerts its anti-inflammatory effects via S1P1, but not via S1P5. Moreover, siponimod also inhibited histone deacetylase, suggesting that siponimod exerts broad anti-inflammatory effects via S1P1 antagonization and histone deacetylase inhibition. Siponimod might suppress disease progression in multiple sclerosis in part via direct inhibition of astroglial CNS neuroinflammation.

    DOI： 10.1016/j.neures.2022.08.003

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  • Phosphorylated CRMP1, axon guidance protein, is a component of spheroids and is involved in axonal pathology in amyotrophic lateral sclerosis. 国際誌

    Yuko Kawamoto, Mikiko Tada, Tetsuya Asano, Haruko Nakamura, Aoi Jitsuki-Takahashi, Hiroko Makihara, Shun Kubota, Shunta Hashiguchi, Misako Kunii, Toshio Ohshima, Yoshio Goshima, Hideyuki Takeuchi, Hiroshi Doi, Fumio Nakamura, Fumiaki Tanaka

    Frontiers in neurology   13   994676 - 994676   2022年

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    記述言語：英語   掲載種別：研究論文（学術雑誌）  

    In amyotrophic lateral sclerosis (ALS), neurodegeneration is characterized by distal axonopathy that begins at the distal axons, including the neuromuscular junctions, and progresses proximally in a "dying back" manner prior to the degeneration of cell bodies. However, the molecular mechanism for distal axonopathy in ALS has not been fully addressed. Semaphorin 3A (Sema3A), a repulsive axon guidance molecule that phosphorylates collapsin response mediator proteins (CRMPs), is known to be highly expressed in Schwann cells near distal axons in a mouse model of ALS. To clarify the involvement of Sema3A-CRMP signaling in the axonal pathogenesis of ALS, we investigated the expression of phosphorylated CRMP1 (pCRMP1) in the spinal cords of 35 patients with sporadic ALS and seven disease controls. In ALS patients, we found that pCRMP1 accumulated in the proximal axons and co-localized with phosphorylated neurofilaments (pNFs), which are a major protein constituent of spheroids. Interestingly, the pCRMP1:pNF ratio of the fluorescence signal in spheroid immunostaining was inversely correlated with disease duration in 18 evaluable ALS patients, indicating that the accumulation of pCRMP1 may precede that of pNFs in spheroids or promote ALS progression. In addition, overexpression of a phospho-mimicking CRMP1 mutant inhibited axonal outgrowth in Neuro2A cells. Taken together, these results indicate that pCRMP1 may be involved in the pathogenesis of axonopathy in ALS, leading to spheroid formation through the proximal progression of axonopathy.

    DOI： 10.3389/fneur.2022.994676

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  • Inhibition of Crmp1 Phosphorylation at Ser522 Ameliorates Motor Function and Neuronal Pathology in Amyotrophic Lateral Sclerosis Model Mice. 国際誌

    Tetsuya Asano, Haruko Nakamura, Yuko Kawamoto, Mikiko Tada, Yayoi Kimura, Hiroshi Takano, Ryoji Yao, Hiroya Saito, Takuya Ikeda, Hiroyasu Komiya, Shun Kubota, Shunta Hashiguchi, Keita Takahashi, Misako Kunii, Kenichi Tanaka, Yoshio Goshima, Fumio Nakamura, Hideyuki Takeuchi, Hiroshi Doi, Fumiaki Tanaka

    eNeuro   9 ( 3 )   2022年

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    記述言語：英語   掲載種別：研究論文（学術雑誌）  

    Amyotrophic lateral sclerosis (ALS) is a rapidly progressive and fatal neurodegenerative disorder that affects upper and lower motor neurons; however, its pathomechanism has not been fully elucidated. Using a comprehensive phosphoproteomic approach, we have identified elevated phosphorylation of Collapsin response mediator protein 1 (Crmp1) at serine 522 in the lumbar spinal cord of ALS model mice overexpressing a human superoxide dismutase mutant (SOD1G93A). We investigated the effects of Crmp1 phosphorylation and depletion in SOD1G93A mice using Crmp1S522A (Ser522→Ala) knock-in (Crmp1ki/ki ) mice in which the S522 phosphorylation site was abolished and Crmp1 knock-out (Crmp1-/-) mice, respectively. Crmp1ki/ki /SOD1G93A mice showed longer latency to fall in a rotarod test while Crmp1-/-/SOD1G93A mice showed shorter latency compared with SOD1G93A mice. Survival was prolonged in Crmp1ki/ki /SOD1G93A mice but not in Crmp1-/-/SOD1G93A mice. In agreement with these phenotypic findings, residual motor neurons and innervated neuromuscular junctions (NMJs) were comparatively well-preserved in Crmp1ki/ki /SOD1G93A mice without affecting microglial and astroglial pathology. Pathway analysis of proteome alterations showed that the sirtuin signaling pathway had opposite effects in Crmp1ki/ki /SOD1G93A and Crmp1-/-/SOD1G93A mice. Our study indicates that modifying CRMP1 phosphorylation is a potential therapeutic strategy for ALS.

    DOI： 10.1523/ENEURO.0133-22.2022

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  • "COVID arm" detected by MR neurography. 国際誌

    Hiroyasu Komiya, Kohei Harada, Ryoji Morishita, Shunta Hashiguchi, Mikiko Tada, Kenichi Tanaka, Hiroshi Doi, Hideyuki Takeuchi, Fumiaki Tanaka

    eNeurologicalSci   25   100377 - 100377   2021年12月

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    記述言語：英語   掲載種別：研究論文（学術雑誌）  

    DOI： 10.1016/j.ensci.2021.100377

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  • SGTA associates with intracellular aggregates in neurodegenerative diseases. 国際誌

    Shun Kubota, Hiroshi Doi, Shigeru Koyano, Kenichi Tanaka, Hiroyasu Komiya, Atsuko Katsumoto, Shingo Ikeda, Shunta Hashiguchi, Haruko Nakamura, Ryoko Fukai, Keita Takahashi, Misako Kunii, Mikiko Tada, Hideyuki Takeuchi, Fumiaki Tanaka

    Molecular brain   14 ( 1 )   59 - 59   2021年3月

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    記述言語：英語   掲載種別：研究論文（学術雑誌）  

    Intracellular aggregates are a common pathological hallmark of neurodegenerative diseases such as polyglutamine (polyQ) diseases, amyotrophic lateral sclerosis (ALS), Parkinson's disease (PD), and multiple system atrophy (MSA). Aggregates are mainly formed by aberrant disease-specific proteins and are accompanied by accumulation of other aggregate-interacting proteins. Although aggregate-interacting proteins have been considered to modulate the formation of aggregates and to be involved in molecular mechanisms of disease progression, the components of aggregate-interacting proteins remain unknown. In this study, we showed that small glutamine-rich tetratricopeptide repeat-containing protein alfa (SGTA) is an aggregate-interacting protein in neurodegenerative diseases. Immunohistochemistry showed that SGTA interacted with intracellular aggregates in Huntington disease (HD) cell models and neurons of HD model mice. We also revealed that SGTA colocalized with intracellular aggregates in postmortem brains of patients with polyQ diseases including spinocerebellar ataxia (SCA)1, SCA2, SCA3, and dentatorubral-pallidoluysian atrophy. In addition, SGTA colocalized with glial cytoplasmic inclusions in the brains of MSA patients, whereas no accumulation of SGTA was observed in neurons of PD and ALS patients. In vitro study showed that SGTA bound to polyQ aggregates through its C-terminal domain and SGTA overexpression reduced intracellular aggregates. These results suggest that SGTA may play a role in the formation of aggregates and may act as potential modifier of molecular pathological mechanisms of polyQ diseases and MSA.

    DOI： 10.1186/s13041-021-00770-1

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  • Case Report: Takotsubo Cardiomyopathy in Bickerstaff Brainstem Encephalitis Triggered by COVID-19. 国際誌

    Mizuki Kimura, Shunta Hashiguchi, Kenichi Tanaka, Manato Hagiwara, Keita Takahashi, Yosuke Miyaji, Hideto Joki, Hiroshi Doi, Michiaki Koga, Hideyuki Takeuchi, Fumiaki Tanaka

    Frontiers in neurology   12   822247 - 822247   2021年

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    記述言語：英語  

    Takotsubo cardiomyopathy (TCM) is a stress-induced cardiomyopathy triggered by critical illness including severe neurological disorders. However, an association between TCM and Bickerstaff brainstem encephalitis (BBE) has rarely been described. During the current coronavirus disease 2019 (COVID-19) pandemic, growing evidence indicates that COVID-19 often leads to various neurological disorders, but there are few reports of an association between COVID-19 and BBE. Here we report a case of TCM associated with BBE triggered by COVID-19, which subsided with immunotherapy for BBE. Both transthoracic echocardiography and electrocardiography led to early and accurate diagnosis of TCM. Sustained hemodynamic instability due to TCM was immediately lessened with immunotherapy whereas additional plasmapheresis and immunotherapy were required to treat BBE. This case indicates that BBE might follow COVID-19 and TCM should be considered when hemodynamic status remains unstable in a patient with BBE.

    DOI： 10.3389/fneur.2021.822247

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  • De novo CACNA1G variants in developmental delay and early-onset epileptic encephalopathies. 国際誌

    Misako Kunii, Hiroshi Doi, Shunta Hashiguchi, Toyojiro Matsuishi, Yasunari Sakai, Mizue Iai, Masaki Okubo, Haruko Nakamura, Keita Takahashi, Atsuko Katsumoto, Mikiko Tada, Hideyuki Takeuchi, Taro Ishikawa, Noriko Miyake, Hirotomo Saitsu, Naomichi Matsumoto, Fumiaki Tanaka

    Journal of the neurological sciences   416   117047 - 117047   2020年9月

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    記述言語：英語   掲載種別：研究論文（学術雑誌）  

    INTRODUCTION: Variants of CACNA1G, which encodes CaV3.1, have been reported to be associated with various neurological disorders. METHODS: Whole-exome sequencing of genomic DNA from 348 Japanese patients with neurodevelopmental disorders and their parents was conducted, and de novo variants of CACNA1G were extracted. The electrophysiological properties of each mutant channel were investigated by voltage-clamp and current-clamp analyses of HEK293T cells overexpressing these channels. RESULTS: Two patients diagnosed with Rett syndrome and West syndrome were found to have known pathological CACNA1G mutations reported in cerebellar ataxia cohorts: c.2881G > A, p.Ala961Thr and c.4591A > G, p.Met1531Val, respectively. One patient with Lennox-Gastaut syndrome was revealed to harbor a previously unreported heterozygous variant: c.3817A > T, p.Ile1273Phe. Clinical symptoms of the two patients with known mutations included severe developmental delay without acquisition of the ability to walk independently. The patient with a potentially novel mutation showed developmental delay, intractable seizures, and mild cerebral atrophy on MRI, but the severity of symptoms was milder than in the former two cases. Electrophysiological study using HEK293T cells demonstrated significant changes of T-type Ca2+ currents by p.Ala961Thr and p.Met1531Val SNVs, which were likely to enhance oscillation of membrane potential at low frequencies. In contrast, p.Ile1273Phe showed no significant effects in our electrophysiological evaluations, with its pathogenesis remaining undetermined. CONCLUSION: De novo variants of CACNA1G explain some neurodevelopmental disorders. Our study further provides information to understand the genotype-phenotype correlations of patients with CACNA1G mutations.

    DOI： 10.1016/j.jns.2020.117047

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  • GGC Repeat Expansion of NOTCH2NLC in Adult Patients with Leukoencephalopathy. 査読 国際誌

    Masaki Okubo, Hiroshi Doi, Ryoko Fukai, Atsushi Fujita, Satomi Mitsuhashi, Shunta Hashiguchi, Hitaru Kishida, Naohisa Ueda, Keisuke Morihara, Akihiro Ogasawara, Yuko Kawamoto, Tatsuya Takahashi, Keita Takahashi, Haruko Nakamura, Misako Kunii, Mikiko Tada, Atsuko Katsumoto, Hiromi Fukuda, Takeshi Mizuguchi, Satoko Miyatake, Noriko Miyake, Junichiro Suzuki, Yasuhiro Ito, Jun Sone, Gen Sobue, Hideyuki Takeuchi, Naomichi Matsumoto, Fumiaki Tanaka

    Annals of neurology   86 ( 6 )   962 - 968   2019年12月

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    記述言語：英語  

    Leukoencephalopathies comprise a broad spectrum of disorders, but the genetic background of adult leukoencephalopathies has rarely been assessed. In this study, we analyzed 101 Japanese patients with genetically unresolved adult leukoencephalopathy using whole-exome sequencing and repeat-primed polymerase chain reaction for detecting GGC expansion in NOTCH2NLC. NOTCH2NLC was recently identified as the cause of neuronal intranuclear inclusion disease. We found 12 patients with GGC expansion in NOTCH2NLC as the most frequent cause of adult leukoencephalopathy followed by NOTCH3 variants in our cohort. Furthermore, we found 1 case with de novo GGC expansion, which might explain the underlying pathogenesis of sporadic cases. ANN NEUROL 2019;86:962-968.

    DOI： 10.1002/ana.25586

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  • Genetic analysis of adult leukoencephalopathy patients using a custom-designed gene panel. 査読

    Kunii M, Doi H, Ishii Y, Ohba C, Tanaka K, Tada M, Fukai R, Hashiguchi S, Kishida H, Ueda N, Kudo Y, Kugimoto C, Nakano T, Udaka N, Miyatake S, Miyake N, Saitsu H, Ito Y, Takahashi K, Nakamura H, Tomita-Katsumoto A, Takeuchi H, Koyano S, Matsumoto N, Tanaka F

    Clinical genetics   94 ( 2 )   232 - 238   2018年8月

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    掲載種別：研究論文（学術雑誌）  

    DOI： 10.1111/cge.13371

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    その他リンク： https://onlinelibrary.wiley.com/doi/full-xml/10.1111/cge.13371

  • Matrin 3 Is a Component of Neuronal Cytoplasmic Inclusions of Motor Neurons in Sporadic Amyotrophic Lateral Sclerosis. 査読 国際誌

    Mikiko Tada, Hiroshi Doi, Shigeru Koyano, Shun Kubota, Ryoko Fukai, Shunta Hashiguchi, Noriko Hayashi, Yuko Kawamoto, Misako Kunii, Kenichi Tanaka, Keita Takahashi, Yuki Ogawa, Ryo Iwata, Shoji Yamanaka, Hideyuki Takeuchi, Fumiaki Tanaka

    The American journal of pathology   188 ( 2 )   507 - 514   2018年2月

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    記述言語：英語  

    Mutations in the MATR3 gene have been identified as a cause of familial amyotrophic lateral sclerosis, but involvement of the matrin 3 (MATR3) protein in sporadic amyotrophic lateral sclerosis (SALS) pathology has not been fully assessed. We immunohistochemically analyzed MATR3 pathology in the spinal cords of SALS and control autopsy specimens. MATR3 immunostaining of the motor neuron nuclei revealed two distinct patterns: mild and strong staining. There were no differences in the ratio of mild versus strong nuclear staining between the SALS and control cases. MATR3-containing neuronal cytoplasmic inclusions (NCIs) were observed in 60% of SALS cases. Most motor neurons with MATR3-positive NCIs exhibited a mild nuclear staining pattern. Although 16.8% of NCIs positive for transactivating response region DNA-binding protein 43 (TDP-43) were estimated as double-labeled by MATR3, no MATR3-positive or TDP-43-negative NCIs were observed. Although a previous study found that MATR3-positive NCIs are present only in cases with C9orf72 hexanucleotide repeat expansion, ubiquitin-positive granular NCIs were not observed in the cerebellum, which have been reported as specific to C9orf72-related ALS. Six ALS cases were confirmed to be negative for the GGGGCC hexanucleotide. Our results reveal that MATR3 is a component of TDP-43-positive NCIs in motor neurons, even in SALS, and indicate the broader involvement of MATR3 in ALS pathology and the heterogeneity of TDP-43-positive NCIs.

    DOI： 10.1016/j.ajpath.2017.10.007

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  • A Case of McLeod Syndrome with A Novel XK Missense Mutation. 国際誌

    Hiroyasu Komiya, Mutsuki Takasu, Shunta Hashiguchi, Eri Uematsu, Ryoko Fukai, Kenichi Tanaka, Mikiko Tada, Hideto Joki, Tatsuya Takahashi, Shigeru Koyano, Hiroshi Doi, Hideyuki Takeuchi, Fumiaki Tanaka

    Movement disorders clinical practice   5 ( 3 )   333 - 336   2018年

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    記述言語：英語  

    DOI： 10.1002/mdc3.12614

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  • Interleukin 10 Level in the Cerebrospinal Fluid as a Possible Biomarker for Lymphomatosis Cerebri.

    Shunta Hashiguchi, Takayuki Momoo, Yoko Murohashi, Masanao Endo, Megumi Shimamura, Takashi Kawasaki, Sachie Kanada, Akinori Nozawa, Mikiko Tada, Shigeru Koyano, Fumiaki Tanaka

    Internal medicine (Tokyo, Japan)   54 ( 12 )   1547 - 52   2015年

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    記述言語：英語   掲載種別：研究論文（学術雑誌）  

    A 71-year-old immunocompetent man developed cognitive decline and gait disturbance. Brain magnetic resonance imaging (MRI) revealed bilateral diffuse leukoencephalopathy without a mass lesion. An analysis of the cerebrospinal fluid (CSF) showed elevated levels of interleukin (IL)-10. The condition of the patient progressively deteriorated, and intravenous high-dose steroids proved ineffective. Detection of non-destructive, diffusely infiltrating, large B-cell lymphoma in biopsy and autopsy specimens led to a diagnosis of lymphomatosis cerebri (LC). On serial MRI, the basal ganglia and white matter lesions increased in parallel with the levels of IL-10. These findings suggest that the IL-10 level in the CSF may represent a potentially useful biomarker for the early diagnosis and monitoring of the disease progression in LC.

    DOI： 10.2169/internalmedicine.54.3283

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  • [Literature review of intravascular lymphomatosis].

    Shigeru Koyano, Shunta Hashiguchi, Fumiaki Tanaka

    Brain and nerve = Shinkei kenkyu no shinpo   66 ( 8 )   927 - 46   2014年8月

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    記述言語：日本語   掲載種別：研究論文（学術雑誌）  

    Intravascular lymphoma (IVL) is a rare form of malignant lymphoma characterized by the selective growth of lymphoma cells within the lumina of vessels, without the involvement of adjacent parenchymal tissue. IVL is predominantly of B-cell lineage, but cases of T-cell or natural killer cell lineage have been described occasionally, predominantly involving the skin. IVL usually affects elderly patients with a poor performance status, elevated serum lactic dehydrogenase levels, anemia, and B symptoms. The clinical presentation varies in different geographical areas, particularly between patients diagnosed in Europe and Asia. In European countries, the Western variant of IVL mainly involves the central nervous system and skin; in particular, there is a "cutaneous variant" limited to the skin. In Asian countries, the Asian variant of IVL predominantly accompanies hemophagocytic syndrome. Identification of this disease is difficult because it presents with non-specific clinical symptoms. Although organ biopsies are mandatory for accurate IVL diagnosis, no standard procedure has been established. An additional random skin biopsy may be useful to diagnose IVL at an early stage. Early diagnosis and treatment can improve the outcome of IVL patients following treatment with rituximab-containing chemotherapy.

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MISC

  • Collet-Sicard症候群を呈したAnterior Condylar Confluence硬膜動静脈瘻の77歳男性例

    西濱 脩平, 古宮 裕泰, 浅野 徹也, 橋口 俊太, 高橋 慶太, 東山 雄一, 土井 宏, 田中 章景

    臨床神経学   65 ( 1 )   56 - 56   2025年1月

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    記述言語：日本語   出版者・発行元：(一社)日本神経学会  

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  • 全身炎症に伴うCCR2陽性マクロファージの中枢神経浸潤がALS病態を促進する

    小笠原 陽大, 竹内 英之, 古宮 裕泰, 小川 有紀, 池田 拓也, 高橋 慶太, 大久保 正紀, 橋口 俊太, 中村 治子, 土井 宏, 田中 章景

    神経免疫学   29 ( 1 )   253 - 253   2024年10月

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    記述言語：日本語   出版者・発行元：(一社)日本神経免疫学会  

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  • 髄液LOTUS濃度を用いた多発性硬化症の病勢把握

    中澤 謙介, 高橋 慶太, 池田 拓也, 古宮 裕泰, 窪田 瞬, 橋口 俊太, 中村 治子, 田中 健一, 土井 宏, 竹内 英之, 田中 章景

    臨床神経学   64 ( Suppl. )   S331 - S331   2024年10月

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    記述言語：日本語   出版者・発行元：(一社)日本神経学会  

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  • 広範なミオキミアを呈した成人発症遺伝性痙性対麻痺(SPG79)の74歳男性例

    豊田 夏実, 古宮 裕泰, 橋口 俊太, 東山 雄一, 宮地 洋輔, 松本 直通, 土井 宏, 田中 章景

    臨床神経生理学   52 ( 5 )   610 - 610   2024年10月

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    記述言語：日本語   出版者・発行元：(一社)日本臨床神経生理学会  

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  • 脊髄小脳変性症のすべて 脊髄小脳変性症 病気の理解と最新の治療について

    橋口 俊太, 土井 宏, 田中 章景

    難病と在宅ケア   30 ( 6 )   28 - 31   2024年9月

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    記述言語：日本語   出版者・発行元：(株)日本プランニングセンター  

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  • Corynebacterium provencenseによる皮下埋込型中心静脈ポート感染の1例

    西垣 哲太, 長谷川 拓也, 鈴木 智代, 川崎 理加, 加藤 英明, 橋口 俊太

    日本感染症学会総会・学術講演会・日本化学療法学会学術集会合同学会プログラム・抄録集   98回・72回   np311 - np311   2024年5月

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    記述言語：日本語   出版者・発行元：日本感染症学会・日本化学療法学会  

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  • 網膜色素変性症および繰り返す脳卒中様発作で発症した神経核内封入体病の82歳女性例

    小林 怜右, 橋口 俊太, 柳泉 茉由莉, 武田 むつき, 小林 絵礼奈, 古宮 裕泰, 東山 雄一, 田中 章景

    臨床神経学   64 ( 3 )   212 - 212   2024年3月

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    記述言語：日本語   出版者・発行元：(一社)日本神経学会  

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  • 両側声帯麻痺を呈し気管切開術を要したβプロペラ蛋白関連神経変性症(BPAN)の57歳女性例

    小林 怜右, 古宮 裕泰, 小林 絵礼奈, 橋口 俊太, 高橋 慶太, 東山 雄一, 土井 宏, 田中 章景

    臨床神経学   63 ( 11 )   775 - 775   2023年11月

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    記述言語：日本語   出版者・発行元：(一社)日本神経学会  

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  • 両側声帯麻痺を呈し気管切開術を要したβプロペラ蛋白関連神経変性症(BPAN)の57歳女性例

    小林 怜右, 古宮 裕泰, 小林 絵礼奈, 橋口 俊太, 高橋 慶太, 東山 雄一, 土井 宏, 田中 章景

    臨床神経学   63 ( 11 )   775 - 775   2023年11月

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    記述言語：日本語   出版者・発行元：(一社)日本神経学会  

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  • 家系内で異なる臨床像を呈しVCP遺伝子バリアントを認めた家族性筋萎縮性側索硬化症の兄弟例

    細田 航平, 古宮 裕泰, 橋口 俊太, 田中 健一, 宮地 洋輔, 土井 宏, 竹内 英之, 田中 章景

    臨床神経学   63 ( 9 )   605 - 605   2023年9月

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    記述言語：日本語   出版者・発行元：(一社)日本神経学会  

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  • 家系内で異なる臨床像を呈しVCP遺伝子バリアントを認めた家族性筋萎縮性側索硬化症の兄弟例

    細田 航平, 古宮 裕泰, 橋口 俊太, 田中 健一, 宮地 洋輔, 土井 宏, 竹内 英之, 田中 章景

    臨床神経学   63 ( 9 )   605 - 605   2023年9月

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    記述言語：日本語   出版者・発行元：(一社)日本神経学会  

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  • 【急性期から在宅まで活用できる!!脳神経内科疾患と看護】(2章)脳神経内科疾患と看護(5)神経難病 フリードライヒ運動失調症(Friedreich病)

    橋口 俊太, 田中 章景

    Brain Nursing   ( 2023夏季増刊 )   219 - 221   2023年8月

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    記述言語：日本語   出版者・発行元：(株)メディカ出版  

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  • 呼吸筋障害と片側声帯麻痺を認めたCharcot-Marie-Tooth病2A型の23歳女性例

    山田 亮, 橋口 俊太, 西町 明浩, 浅野 徹也, 小林 絵礼奈, 田中 健一, 多田 美紀子, 田中 章景

    臨床神経学   63 ( 3 )   175 - 175   2023年3月

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    記述言語：日本語   出版者・発行元：(一社)日本神経学会  

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  • 腫瘤を形成せず慢性髄膜脳炎の経過を呈した中枢神経原発低悪性度B細胞リンパ腫の45歳男性例

    西町 明浩, 橋口 俊太, 田中 健一, 宮地 洋輔, 多田 美紀子, 土井 宏, 竹内 英之, 田中 章景

    臨床神経学   62 ( 12 )   966 - 966   2022年12月

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    記述言語：日本語   出版者・発行元：(一社)日本神経学会  

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  • SCA42モデルマウスに対するエトサクシミドの治療効果

    大久保 正紀, 土井 宏, 橋口 俊太, 高橋 慶太, 田中 健一, 竹内 英之, 石川 太郎, 田中 章景

    神経治療学   39 ( 6 )   S234 - S234   2022年10月

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    記述言語：日本語   出版者・発行元：(一社)日本神経治療学会  

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  • CRMP1のリン酸化阻害は筋萎縮性側索硬化症モデルマウスの生存期間,運動機能の改善をもたらす

    浅野 徹也, 中村 治子, 川本 裕子, 木村 弥生, 高野 洋志, 八尾 良司, 橋口 俊太, 高橋 慶太, 田中 健一, 五嶋 良郎, 中村 史雄, 竹内 英之, 土井 宏, 田中 章景

    神経治療学   39 ( 6 )   S255 - S255   2022年10月

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    記述言語：日本語   出版者・発行元：(一社)日本神経治療学会  

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  • Nogo受容体の内因性アンタゴニストであるLOTUSはALSモデルマウスの症状を改善する

    池田 拓也, 高橋 慶太, 橋口 俊太, 田中 健一, 土井 宏, 竹居 光太郎, 竹内 英之, 田中 章景

    神経治療学   39 ( 6 )   S255 - S255   2022年10月

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    記述言語：日本語   出版者・発行元：(一社)日本神経治療学会  

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  • 舞踏運動を主徴とし、抗リン脂質抗体と抗amphiphysin抗体が陽性であった69歳男性例

    森下 良志, 原田 康平, 古宮 裕泰, 橋口 俊太, 田中 健一, 多田 美紀子, 土井 宏, 田中 章景

    臨床神経学   62 ( 8 )   676 - 676   2022年8月

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    記述言語：日本語   出版者・発行元：(一社)日本神経学会  

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  • 舞踏運動を主徴とし、抗リン脂質抗体と抗amphiphysin抗体が陽性であった69歳男性例

    森下 良志, 原田 康平, 古宮 裕泰, 橋口 俊太, 田中 健一, 多田 美紀子, 土井 宏, 田中 章景

    臨床神経学   62 ( 8 )   676 - 676   2022年8月

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    記述言語：日本語   出版者・発行元：(一社)日本神経学会  

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  • たこつぼ型心筋症を合併したBickerstaff脳幹脳炎の68歳女性例

    木村 瑞希, 橋口 俊太, 田中 健一, 高橋 慶太, 宮地 洋輔, 上木 英人, 土井 宏, 竹内 英之, 田中 章景

    神経治療学   37 ( 6 )   S248 - S248   2020年10月

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    記述言語：日本語   出版者・発行元：(一社)日本神経治療学会  

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  • 研究者の最新動向 脊髄小脳失調症新規モデルマウスを用いた病態解析

    土井 宏, 橋口 俊太, 中村 行宏, 石川 太郎, 田中 章景

    Precision Medicine   2 ( 13 )   1260 - 1266   2019年12月

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    記述言語：日本語   出版者・発行元：(株)北隆館  

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  • 特発性肥厚性硬膜炎に脳静脈洞血栓症を合併した41歳男性例

    橋口 俊太, 川本 裕子, 城村 裕司, 岡田 雅仁, 田中 章景

    脳卒中   38 ( 4 )   272 - 275   2016年7月

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  • 当院にて入院加療した悪性症候群の臨床的検討

    橋口 俊太, 小島 麻里, 植松 絵里, 田中 章景

    臨床神経学   55 ( Suppl. )   S457 - S457   2015年12月

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    記述言語：日本語   出版者・発行元：(一社)日本神経学会  

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  • めまいを主訴として来院した脳静脈洞血栓症の1例

    春日井 裕美, 高橋 耕平, 森 浩介, 城村 裕司, 川本 裕子, 橋口 俊太

    日本救急医学会関東地方会雑誌   35 ( 2 )   415 - 420   2014年12月

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    記述言語：日本語   出版者・発行元：日本救急医学会-関東地方会  

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  • パーキンソン病症例における血中不飽和脂肪酸の検討

    岡田 雅仁, 橋口 俊太, 川本 裕子, 城村 裕司

    臨床神経学   54 ( Suppl. )   S88 - S88   2014年12月

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    記述言語：日本語   出版者・発行元：(一社)日本神経学会  

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  • 若年発症の筋萎縮性側索硬化症におけるスポーツ歴

    城村 裕司, 川本 裕子, 橋口 俊太, 田中 章景

    臨床神経学   54 ( Suppl. )   S147 - S147   2014年12月

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    記述言語：日本語   出版者・発行元：(一社)日本神経学会  

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  • 眼で見る神経内科 多発微小脳出血を合併した顕微鏡的多発血管炎

    橋口 俊太, 工藤 洋祐, 上田 直久, 黒岩 義之, 田中 章景

    神経内科   81 ( 4 )   460 - 462   2014年10月

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    記述言語：日本語   出版者・発行元：(有)科学評論社  

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  • 卵巣奇形腫を合併した抗NMDAR抗体陰性、抗GluR抗体陽性自己免疫性辺縁系脳炎の34歳女性例

    橋口 俊太, 川本 裕子, 城村 裕司, 岡田 雅仁, 田中 惠子, 高橋 幸利

    臨床神経学   54 ( 8 )   695 - 695   2014年8月

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    記述言語：日本語   出版者・発行元：(一社)日本神経学会  

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  • 特発性肥厚性硬膜炎に静脈洞血栓症を合併した41歳男性例

    山田 択, 橋口 俊太, 子島 俊太郎, 川本 裕子, 城村 裕司, 岡田 雅仁

    共済医報   63 ( 3 )   280 - 280   2014年8月

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    記述言語：日本語   出版者・発行元：国家公務員共済組合連合会  

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  • 卵巣奇形腫を合併した抗NMDAR抗体陰性、抗GluR抗体陽性、自己免疫性辺縁系脳炎の34歳女性例

    橋口 俊太, 川本 裕子, 城村 裕司, 岡田 雅仁

    共済医報   63 ( 3 )   281 - 281   2014年8月

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    記述言語：日本語   出版者・発行元：国家公務員共済組合連合会  

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  • 【神経疾患の性差をみる】Parkinson病と性差

    黒岩 義之, 馬場 泰尚, 川端 雄一, 橋口 俊太, 田中 章景

    神経内科   81 ( 2 )   145 - 148   2014年8月

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    記述言語：日本語   出版者・発行元：(有)科学評論社  

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  • 神経変性疾患患者の脳MRIにおける年間萎縮率Annual Atrophic Rate(AAR)

    黒岩 義之, 堀 寛子, 川端 雄一, 橋口 俊太, 田中 章景, 児矢野 繁, 鈴木 ゆめ, 上田 直久, 上木 英人, 東山 雄一, 藤野 公裕, 黒川 隆史, 馬場 泰尚

    臨床神経学   53 ( 12 )   1437 - 1437   2013年12月

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    記述言語：日本語   出版者・発行元：(一社)日本神経学会  

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  • CIDP、GBSにおける免疫グロブリン大量静注療法前後での電流知覚閾値(CPT)測定の有用性

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