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森野豊之

徳島大学

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2024年5月15日更新

職名: 教授
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電子メール: morino@tokushima-u.ac.jp
学歴: 研究者総覧に該当データはありませんでした。
学位: 博士(医学) (広島大学) (2000年2月)
職歴・経歴: 2021/6: 徳島大学教授, 大学院医歯薬学研究部

専門分野・研究分野: 遺伝学 (Genetics)

研究者総覧で最新データを確認する

2024年5月15日更新

専門分野・研究分野: 遺伝学 (Genetics)
担当経験のある授業科目: 先端医学 (学部)
公衆衛生学 (学部)
助産学特論Ⅱ(生命倫理学) (大学院)
医学概論 (共通教育)
基礎医学 (学部)
技術英語入門 (学部)
研究室配属 (学部)
遺伝・公衆衛生 (学部)
遺伝学 (学部)
遺伝情報医学 (大学院)
遺伝情報医学演習 (大学院)
指導経験: 研究者総覧に該当データはありませんでした。

研究者総覧で最新データを確認する

2024年5月15日更新

専門分野・研究分野: 遺伝学 (Genetics)

研究テーマ: 遺伝性疾患の原因遺伝子検索と病態解明 (遺伝学 (genetics), 神経変性 (neurodegeneration), ゲノム編集 (genome editing), 遺伝子工学 (genetic engineering), 遺伝子治療 (gene therapy))

著書

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論文

Takafumi Tomenaga, Shinobu Minatani, Hiroto Namba, Akitoshi Takeda, Takahito Yoshizaki, Joji Kawabe, KEYOUMU NAZERE, Hiroyuki Morino, Makoto Higuchi, Tomoyasu Matsubara, Hiroyuki Hatsuta, Masato Hasegawa, Shigeo Murayama and Yoshiaki Itoh :
An autopsy case of type A FTLD-TDP with a GRN mutation presenting with the logopenic variant of primary progressive aphasia at onset and with corticobasal syndrome subsequently.,
Neuropathology, 2024.

(要約): A 68-year-old woman presented with difficulty finding words and writing characters. Neurological examination led to clinical diagnosis at onset of the logopenic variant of primary progressive aphasia accompanied with ideomotor apraxia, visuospatial agnosia on the right, and Gerstmann syndrome. Bradykinesia and rigidity on the right with shuffling gait developed after one year. Treatment with L-dopa had no effect. The patient was diagnosed with corticobasal syndrome (CBS). Brain magnetic resonance imaging revealed diffuse cortical atrophy dominantly on the left, especially in the temporal, parietal, and occipital lobes. Positron emission tomography did not reveal any significant accumulation of amyloid β or tau protein. She died five years later. Neuropathological examination revealed diffuse cortical atrophy with severe neuronal loss and fibrous gliosis in the cortex. Neuronal cytoplasmic inclusions, short dystrophic neurites, and, most notably, neuronal intranuclear inclusions, all immunoreactive for phosphorylated TDP-43, were observed. Western blotting revealed a full length and fragments of phosphorylated TDP-43 at 45 and 23kDa, respectively, confirming the pathological diagnosis of type A FTLD-TDP. Whole exome sequencing revealed a pathogenic mutation in GRN (c.87dupC). FTLD-TDP should be included in the differential diagnosis of CBS.
(出版サイトへのリンク): ● Publication site (DOI): 10.1111/neup.12980
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38715398; ● Search Scopus @ Elsevier (PMID): 38715398; ● Search Scopus @ Elsevier (DOI): 10.1111/neup.12980

(DOI: 10.1111/neup.12980, PubMed: 38715398) Hiroyuki Morino, Takashi Kurashige, Yukiko Matsuda, Maiko Ono, Naruhiko Sahara, Tomohiro Miyasaka, Yoshiyuki Soeda, Hitoshi Shimada, Yu Yamazaki, Tetsuya Takahashi, Yuishin Izumi, Hidefumi Ito, Hirofumi Maruyama, Makoto Higuchi, Koji Arihiro, Tetsuya Suhara, Akihiko Takashima and Hideshi Kawakami :
Clinical and Pathological Features of FTDP-17 with MAPT p.K298_H299insQ Mutation.,
Movement Disorders Clinical Practice, 2024.

(要約): This study confirmed that the insACA mutation caused FTDP-17. The affected patients showed symptoms resembling Parkinson's disease initially and symptoms of progressive supranuclear palsy later. Despite the initial clinical diagnosis of frontotemporal dementia in the autopsy case, the spread of lesions could explain the process of progressive supranuclear palsy. The study of more cases in the future will help clarify the common pathogenesis of MAPT mutations or specific pathogeneses of each mutation.
(出版サイトへのリンク): ● Publication site (DOI): 10.1002/mdc3.14042
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38605589; ● Search Scopus @ Elsevier (PMID): 38605589; ● Search Scopus @ Elsevier (DOI): 10.1002/mdc3.14042

(DOI: 10.1002/mdc3.14042, PubMed: 38605589) Mizuho Kittaka, Noriyoshi Mizuno, Hiroyuki Morino, Tetsuya Yoshimoto, Tianli Zhu, Sheng Liu, Ziyi Wang, Kotoe Mayahara, Kyohei Iio, Kaori Kondo, Toshio Kondo, Tatsuhide Hayashi, Sarah Coghlan, Yayoi Teno, Phung Andrew Anh Doan, Marcus Levitan, B Roy Choi, Shinji Matsuda, Kazuhisa Ouhara, Jun Wan, M Annelise Cassidy, Stephane Pelletier, Sheela Nampoothiri, J Andoni Urtizberea, G Alexander Robling, Mitsuaki Ono, Hideshi Kawakami, J Ernst Reichenberger and Yasuyoshi Ueki :
Loss-of-function OGFRL1 variants identified in autosomal recessive cherubism families.,
JBMR Plus, Vol.8, No.6, 2024.

(要約): Cherubism (OMIM 118400) is a rare craniofacial disorder in children characterized by destructive jawbone expansion due to the growth of inflammatory fibrous lesions. Our previous studies have shown that gain-of-function mutations in SH3 domain-binding protein 2 (SH3BP2) are responsible for cherubism and that a knock-in mouse model for cherubism recapitulates the features of cherubism, such as increased osteoclast formation and jawbone destruction. To date, SH3BP2 is the only gene identified to be responsible for cherubism. Since not all patients clinically diagnosed with cherubism had mutations in SH3BP2, we hypothesized that there may be novel cherubism genes and that these genes may play a role in jawbone homeostasis. Here, using whole exome sequencing, we identified homozygous loss-of-function variants in the opioid growth factor receptor like 1 (OGFRL1) gene in 2 independent autosomal recessive cherubism families from Syria and India. The newly identified pathogenic homozygous variants were not reported in any variant databases, suggesting that OGFRL1 is a novel gene responsible for cherubism. Single cell analysis of mouse jawbone tissue revealed that Ogfrl1 is highly expressed in myeloid lineage cells. We generated OGFRL1 knockout mice and mice carrying the Syrian frameshift mutation to understand the in vivo role of OGFRL1. However, neither mouse model recapitulated human cherubism or the phenotypes exhibited by SH3BP2 cherubism mice under physiological and periodontitis conditions. Unlike bone marrow-derived M-CSF-dependent macrophages (BMMs) carrying the SH3BP2 cherubism mutation, BMMs lacking OGFRL1 or carrying the Syrian mutation showed no difference in TNF- mRNA induction by LPS or TNF- compared to WT BMMs. Osteoclast formation induced by RANKL was also comparable. These results suggest that the loss-of-function effects of OGFRL1 in humans differ from those in mice and highlight the fact that mice are not always an ideal model for studying rare craniofacial bone disorders.
(出版サイトへのリンク): ● Publication site (DOI): 10.1093/jbmrpl/ziae050
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38699440; ● Search Scopus @ Elsevier (PMID): 38699440; ● Search Scopus @ Elsevier (DOI): 10.1093/jbmrpl/ziae050

(DOI: 10.1093/jbmrpl/ziae050, PubMed: 38699440) Hidetada Yamada, Yu Yamazaki, Yoshiko Takebayashi, Kyosuke Yazawa, Miwako Sasanishi, Atsuko Motoda, Masahiro Nakamori, Hiroyuki Morino, Tetsuya Takahashi and Hirofumi Maruyama :
The long-term effects of heated tobacco product exposure on the central nervous system in a mouse model of prodromal Alzheimer's disease.,
Scientific Reports, Vol.14, No.1, 2024.

(要約): Heated tobacco products (HTPs) have emerged as novel alternatives to conventional cigarettes (CCs), marketed by the tobacco industry as having a reduced potential for harm. Nevertheless, a significant dearth of information remains regarding the long-term effects of HTPs on the central nervous system (CNS). Here, we sought to shed light on the repercussions of prolonged exposure to HTPs on the CNS, employing a mouse model mimicking prodromal Alzheimer's disease (AD). Our study entailed subjecting App knock-in mice to 16 weeks of HTP exposure, administered 5 days per week, with serum cotinine concentration serving as confirmation of HTP exposure within this model. Histological analysis, aimed at assessing amyloid pathology, unveiled a minimal impact attributable to HTPs. However, exploration of differentially expressed genes in the cerebral cortex, using unadjusted p values, indicated an association between HTP exposure and non-inflammatory pathways, specifically linked to neurohypophyseal and neuropeptide hormone activity within the CNS. Of note, similar results have already been observed after exposure to CCs in vivo. Our study not only contributes insights into the potential non-inflammatory effects of HTPs within the context of AD pathogenesis but also underscores the significance of continued research to comprehend the full scope of their impact on the CNS.
(キーワード): Animals / Mice / Alzheimer Disease / Central Nervous System / Disease Models, Animal / Amyloidogenic Proteins / Tobacco Products / Electronic Nicotine Delivery Systems
(出版サイトへのリンク): ● Publication site (DOI): 10.1038/s41598-023-50941-4
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38167640; ● Search Scopus @ Elsevier (PMID): 38167640; ● Search Scopus @ Elsevier (DOI): 10.1038/s41598-023-50941-4

(DOI: 10.1038/s41598-023-50941-4, PubMed: 38167640) Mai Kikumoto, Takashi Kurashige, Tomohiko Ohshita, Kodai Kume, Osamu Kikumoto, Tomohisa Nezu, Shiro Aoki, Kazuhide Ochi, Hiroyuki Morino, Eiichi Nomura, Hiroshi Yamashita, Mayumi Kaneko, Hirofumi Maruyama and Hideshi Kawakami :
'Raisin bread sign' feature of pontine autosomal dominant microangiopathy and leukoencephalopathy.,
Brain Communications, Vol.5, No.6, fcad281, 2023.

(要約): 3'UTR was observed in two patients with familial small vessel disease and the two selected patients, thereby confirming the pontine autosomal dominant microangiopathy and leukoencephalopathy diagnosis. Furthermore, postmortem examination showed that the distribution of thickened media tunica and hyalinized vessels was different from that in lacunar infarctions. The appearance of characteristic multiple oval small infarctions in the pons, which resemble raisin bread, enable us to make a diagnosis of pontine autosomal dominant microangiopathy and leukoencephalopathy. This feature, for which we coined the name 'raisin bread sign', was also correlated to the pathological changes.
(出版サイトへのリンク): ● Publication site (DOI): 10.1093/braincomms/fcad281
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37953842; ● Search Scopus @ Elsevier (PMID): 37953842; ● Search Scopus @ Elsevier (DOI): 10.1093/braincomms/fcad281

(DOI: 10.1093/braincomms/fcad281, PubMed: 37953842) Kodai Kume, Takashi Kurashige, Keiko Muguruma, Hiroyuki Morino, Yui Tada, Mai Kikumoto, Tatsuo Miyamoto, Natsuko Silvia Akutsu, Yukiko Matsuda, Shinya Matsuura, Masahiro Nakamori, Ayumi Nishiyama, Rumiko Izumi, Tetsuya Niihori, Masashi Ogasawara, Nobuyuki Eura, Tamaki Kato, Mamoru Yokomura, Yoshiaki Nakayama, Hidefumi Ito, Masataka Nakamura, Kayoko Saito, Yuichi Riku, Yasushi Iwasaki, Hirofumi Maruyama, Yoko Aoki, Ichizo Nishino, Yuishin Izumi, Masashi Aoki and Hideshi Kawakami :
CGG repeat expansion in LRP12 in amyotrophic lateral sclerosis.,
American Journal of Human Genetics, Vol.110, No.7, 1086-1097, 2023.

(要約): Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disorder characterized by the degeneration of motor neurons. Although repeat expansion in C9orf72 is its most common cause, the pathogenesis of ALS isn't fully clear. In this study, we show that repeat expansion in LRP12, a causative variant of oculopharyngodistal myopathy type 1 (OPDM1), is a cause of ALS. We identify CGG repeat expansion in LRP12 in five families and two simplex individuals. These ALS individuals (LRP12-ALS) have 61-100 repeats, which contrasts with most OPDM individuals with repeat expansion in LRP12 (LRP12-OPDM), who have 100-200 repeats. Phosphorylated TDP-43 is present in the cytoplasm of iPS cell-derived motor neurons (iPSMNs) in LRP12-ALS, a finding that reproduces the pathological hallmark of ALS. RNA foci are more prominent in muscle and iPSMNs in LRP12-ALS than in LRP12-OPDM. Muscleblind-like 1 aggregates are observed only in OPDM muscle. In conclusion, CGG repeat expansions in LRP12 cause ALS and OPDM, depending on the length of the repeat. Our findings provide insight into the repeat length-dependent switching of phenotypes.
(キーワード): 神経変性 (neurodegeneration) / 遺伝学 (genetics) / 神経系 (nervous system) / 遺伝子疾患 (gene disorders) / 神経科学 (neuroscience)
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.ajhg.2023.05.014
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37339631; ● Summary page in Scopus @ Elsevier: 2-s2.0-85164273883

(DOI: 10.1016/j.ajhg.2023.05.014, PubMed: 37339631, Elsevier: Scopus) Shotaro Haji, Ryosuke Miyamoto, Hiroyuki Morino, Yusuke Osaki, Seijiro Tsuji, Ichizo Nishino, Masahiro Abe and Yuishin Izumi :
Autosomal Recessive Spinocerebellar Ataxia Type 9 With a Response to Phosphate Repletion: A Case Report.,
Neurology. Genetics, Vol.9, No.3, 2023.

(要約): This provides Class IV evidence. This is a single observational study without controls.
(出版サイトへのリンク): ● Publication site (DOI): 10.1212/NXG.0000000000200070
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37529414; ● Search Scopus @ Elsevier (PMID): 37529414; ● Search Scopus @ Elsevier (DOI): 10.1212/NXG.0000000000200070

(DOI: 10.1212/NXG.0000000000200070, PubMed: 37529414) Shotaro Haji, Koji Fujita, Ryosuke Oki, Yusuke Osaki, Ryosuke Miyamoto, Hiroyuki Morino, Seiichi Nagano, Naoki Atsuta, Yuki Kanazawa, Yuki Matsumoto, Atsuko Arisawa, Hisashi Kawai, Yasutaka Sato, Satoshi Sakaguchi, Kenta Yagi, Tatsuto Hamatani, Tatsuo Kagimura, Hiroaki Yanagawa, Hideki Mochizuki, Manabu Doyu, Gen Sobue, Masafumi Harada and Yuishin Izumi :
An Exploratory Trial of EPI-589 in Amyotrophic Lateral Sclerosis (EPIC-ALS): Protocol for a Multicenter, Open-Labeled, 24-Week, Single-Group Study,
JMIR Research Protocols, Vol.12, e42032, 2023.

(要約): Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder, with its currently approved drugs, including riluzole and edaravone, showing limited therapeutic effects. Therefore, safe and effective drugs are urgently necessary. EPI-589 is an orally available, small-molecule, novel redox-active agent characterized by highly potent protective effects against oxidative stress with high blood-brain barrier permeability. Given the apparent oxidative stress and mitochondrial dysfunction involvement in the pathogenesis of ALS, EPI-589 may hold promise as a therapeutic agent. This protocol aims to describe the design and rationale for the EPI-589 Early Phase 2 Investigator-Initiated Clinical Trial for ALS (EPIC-ALS). EPIC-ALS is an explorative, open-labeled, single-arm trial that evaluates the safety and tolerability of EPI-589 in patients with ALS. This trial consists of 12-week run-in, 24-week treatment, and 4-week follow-up periods. Patients will receive 500 mg of EPI-589 3 times daily over the 24-week treatment period. Clinical assessments include the mean monthly change of Amyotrophic Lateral Sclerosis Functional Rating Scale-Revised total score. The biomarkers are selected to analyze the effect on oxidative stress and neuronal damage. The plasma biomarkers are 8-hydroxy-2'-deoxyguanosine (8-OHdG), 3-nitrotyrosine (3-NT), neurofilament light chain (NfL), phosphorylated neurofilament heavy chain (pNfH), homocysteine, and creatinine. The cerebrospinal fluid biomarkers are 8-OHdG, 3-NT, NfL, pNfH, and ornithine. The magnetic resonance biomarkers are fractional anisotropy in the corticospinal tract and N-acetylaspartate in the primary motor area. This trial began data collection in September 2021 and is expected to be completed in October 2023. This study can provide useful data to understand the characteristics of EPI-589. Japan Primary Registries Network jRCT2061210031; tinyurl.com/2p84emu6. DERR1-10.2196/42032.
(徳島大学機関リポジトリ): ● Metadata: 118866
(出版サイトへのリンク): ● Publication site (DOI): 10.2196/42032
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36716091; ● Summary page in Scopus @ Elsevier: 2-s2.0-85149143248

(徳島大学機関リポジトリ: 118866, DOI: 10.2196/42032, PubMed: 36716091, Elsevier: Scopus) Hidetada Yamada, Shuichiro Neshige, Hiroyuki Morino and Hirofumi Maruyama :
Extubation failure due to atypical parkinsonism with negligible motor and variable non-motor symptoms associated with a variant of DCTN1.,
Internal and Emergency Medicine, 2022.

(出版サイトへのリンク): ● Publication site (DOI): 10.1007/s11739-022-03105-7
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36504048; ● Search Scopus @ Elsevier (PMID): 36504048; ● Search Scopus @ Elsevier (DOI): 10.1007/s11739-022-03105-7

(DOI: 10.1007/s11739-022-03105-7, PubMed: 36504048) Hidetada Yamada, Masahiro Nakamori, Junichiro Kuga, Akemi Hironaka, Takamichi Sugimoto, Hiroki Ueno, Tomohiko Ohshita, Hiroyuki Morino and Hirofumi Maruyama :
Nerve Ultrasonography for the Diagnosis and Evaluation of Neuralgic Amyotrophy: A Case Report.,
Internal Medicine, 2022.

(要約): Neuralgic amyotrophy (NA) is a peripheral nervous system disorder involving multifocal distribution. Although nerve ultrasonography has shown potential for detecting NA lesions, no established detection method exists for distal forearm NA. A 59-year-old man presented with weakness of the muscles innervated by the left posterior interosseous nerve (PIN), median nerve (MN), anterior interosseous nerve (AIN), and ulnar nerve (UN), following severe left shoulder pain. This case suggests that nerve ultrasonography can help accurately diagnose distal forearm NA.
(出版サイトへのリンク): ● Publication site (DOI): 10.2169/internalmedicine.0005-22
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36351573; ● Search Scopus @ Elsevier (PMID): 36351573; ● Search Scopus @ Elsevier (DOI): 10.2169/internalmedicine.0005-22

(DOI: 10.2169/internalmedicine.0005-22, PubMed: 36351573) Takashi Kurashige, Hiroyuki Morino, Hiroki Ueno, Tomomi Murao, Tomoaki Watanabe, Takao Hinoi, Ichizo Nishino, Tsuyoshi Torii and Hirofumi Maruyama :
Gastrointestinal cancer occurs as extramuscular manifestation in FSHD1 patients.,
Journal of Human Genetics, 2022.

(要約): Facioscapulohumeral dystrophy type1 (FSHD1) patients with a shortened D4Z4 repeat containing the DUX4 gene have a broad spectrum of clinical manifestations. In addition, high expression of DUX4 protein with an aberrant C terminus is frequently identified in B cell acute lymphoblastic leukemia. We investigated clinical manifestations in 31 FSHD1 patients and 30 non-affected individuals. Gastrointestinal cancers (gastric and colorectal cancers) increased after the age of 40 years and were more frequently observed in FSHD1 patients (n = 10) than in non-affected individuals (n = 2, p = 0.0217), though the incidence of cancers occurring in non-gastrointestinal tissues of FSHD1 patients was the same as that of non-affected individuals (p > 0.999). These comorbidities of FSHD1 patients were not associated with D4Z4 repeat number. Our results suggest that gastrointestinal cancers are among the extramuscular manifestations of adult FSHD1 patients, and do not depend on D4Z4 repeat number.
(徳島大学機関リポジトリ): ● Metadata: 118058
(出版サイトへのリンク): ● Publication site (DOI): 10.1038/s10038-022-01095-0
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36336708; ● Search Scopus @ Elsevier (PMID): 36336708; ● Search Scopus @ Elsevier (DOI): 10.1038/s10038-022-01095-0

(徳島大学機関リポジトリ: 118058, DOI: 10.1038/s10038-022-01095-0, PubMed: 36336708) Takashi Kurashige, Hiroyuki Morino, Tomomi Murao, Yuishin Izumi, Tomohito Sugiura, Kazuya Kuraoka, Hideshi Kawakami, Tsuyoshi Torii and Hirofumi Maruyama :
TDP-43 Accumulation Within Intramuscular Nerve Bundles of Patients With Amyotrophic Lateral Sclerosis.,
JAMA Neurology, Vol.79, No.7, 693-701, 2022.

(要約): Results of this dual case-control and retrospective cohort study suggest that axonal pTDP-43 accumulations may be characteristic for patients with ALS. As such findings precede clinical fulfillment of the Gold Coast criteria, TDP-43 in nerve bundles may be a novel diagnostic biomarker for ALS.
(キーワード): Aged / Amyotrophic Lateral Sclerosis / Case-Control Studies / Cohort Studies / DNA-Binding Proteins / Humans / Male / Middle Aged / Retrospective Studies
(出版サイトへのリンク): ● Publication site (DOI): 10.1001/jamaneurol.2022.1113
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35604654; ● Search Scopus @ Elsevier (PMID): 35604654; ● Search Scopus @ Elsevier (DOI): 10.1001/jamaneurol.2022.1113

(DOI: 10.1001/jamaneurol.2022.1113, PubMed: 35604654) Keyoumu Nazere, Tetsuya Takahashi, Naoyuki Hara, Kazuki Muguruma, Masahiro Nakamori, Yu Yamazaki, Hiroyuki Morino and Hirofumi Maruyama :
Amyloid Beta Is Internalized via Macropinocytosis, an HSPG- and Lipid Raft-Dependent and Rac1-Mediated Process,
Frontiers in Molecular Neuroscience, Vol.15, 2022.

(徳島大学機関リポジトリ): ● Metadata: 117735
(出版サイトへのリンク): ● Publication site (DOI): 10.3389/fnmol.2022.804702
(文献検索サイトへのリンク): ● Summary page in Scopus @ Elsevier: 2-s2.0-85125185487

(徳島大学機関リポジトリ: 117735, DOI: 10.3389/fnmol.2022.804702, Elsevier: Scopus) Kenichi Ishikawa, Mutsuko Araki, Yoshito Nagano, Atsuko Motoda, Takeo Shishido, Takashi Kurashige, Tetsuya Takahashi, Hiroyuki Morino, Hideshi Kawakami, Masayasu Matsumoto and Hirofumi Maruyama :
Knockdown of optineurin controls C2C12 myoblast differentiation via regulating myogenin and MyoD expressions.,
Differentiation; Research in Biological Diversity, Vol.123, 1-8, 2021.

(要約): Mutations in optineurin (OPTN) have been identified in a small proportion of sporadic and familial amyotrophic lateral sclerosis (ALS) cases. Recent evidences suggest that OPTN would be involved in not only the pathophysiological mechanisms of motor neuron death of ALS but also myofiber degeneration of sporadic inclusion body myositis. However, the detailed role of OPTN in muscle remains unclear. Initially, we showed that OPTN expression levels were significantly increased in the denervated muscles of mice, suggesting that OPTN may be involved in muscle homeostasis. To reveal the molecular role of OPTN in muscle atrophy, we used cultured C2C12 myotubes treated with tumor necrosis factor-like inducer of apoptosis (TWEAK) as an in vitro model of muscle atrophy. Our data showed that OPTN had no effect on the process of muscle atrophy in this model. On the other hand, we found that myogenic differentiation was affected by OPTN. Immunoblotting analysis showed that OPTN protein levels gradually decreased during C2C12 differentiation. Furthermore, OPTN knockdown inhibited C2C12 differentiation, accompanied by reduction of mRNA and protein expression levels of myogenin and MyoD. These findings suggested that OPTN may have a novel function in muscle homeostasis and play a role in the pathogenesis of neuromuscular diseases.
(キーワード): Animals / Cell Cycle Proteins / Cell Differentiation / Membrane Transport Proteins / Mice / Muscular Atrophy / MyoD Protein / Myoblasts / Myogenin / Transcription Factor TFIIIA
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.diff.2021.11.004
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34844057; ● Search Scopus @ Elsevier (PMID): 34844057; ● Search Scopus @ Elsevier (DOI): 10.1016/j.diff.2021.11.004

(DOI: 10.1016/j.diff.2021.11.004, PubMed: 34844057) Megumi Toko, Tomohiko Ohshita, Takashi Kurashige, Hiroyuki Morino, Kodai Kume, Hiroshi Yamashita, Gen Sobue, Yasushi Iwasaki, Jun Sone, Hideshi Kawakami and Hirofumi Maruyama :
FXTAS is difficult to differentiate from neuronal intranuclear inclusion disease through skin biopsy: a case report.,
BMC Neurology, Vol.21, No.1, 2021.

(要約): The patient underwent neurological assessment and examinations, including laboratory tests, electrophysiologic test, imaging, skin biopsy, and genetic test. A brain MRI showed hyperintensity lesions along the corticomedullary junction on diffusion-weighted imaging (DWI) in addition to middle cerebellar peduncle sign (MCP sign). We suspected NIID from the clinical picture and the radiological findings, and performed a skin biopsy. The skin biopsy specimen showed ubiquitin- and p62-positive intranuclear inclusions, suggesting NIID. However, a genetic analysis for NIID using repeat-primed polymerase chain reaction (RP-PCR) revealed no expansion detected in the Notch 2 N-terminal like C (NOTCH2NLC) gene. We then performed genetic analysis for FXTAS using RP-PCR, which revealed a repeat CGG/GGC expansion in the FMRP translational regulator 1 (FMR1) gene. The number of repeats was 83. We finally diagnosed the patient with FXTAS rather than NIID.
(キーワード): Ataxia / Biopsy / Fragile X Mental Retardation Protein / Fragile X Syndrome / Humans / Intranuclear Inclusion Bodies / Neurodegenerative Diseases / Tremor
(出版サイトへのリンク): ● Publication site (DOI): 10.1186/s12883-021-02425-z
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34641814; ● Search Scopus @ Elsevier (PMID): 34641814; ● Search Scopus @ Elsevier (DOI): 10.1186/s12883-021-02425-z

(DOI: 10.1186/s12883-021-02425-z, PubMed: 34641814) Mai Kikumoto, Tomohisa Nezu, Yuji Shiga, Atsuko Motoda, Megumi Toko, Takashi Kurashige, Hiroki Ueno, Tetsuya Takahashi, Hiroyuki Morino, Jun Sone, Yasushi Iwasaki, Gen Sobue and Hirofumi Maruyama :
Case of Neuronal Intranuclear Inclusion Disease With Dynamic Perfusion Changes Lacking Typical Signs on Diffusion-Weighted Imaging.,
Neurology. Genetics, Vol.7, No.4, 2021.

(出版サイトへのリンク): ● Publication site (DOI): 10.1212/NXG.0000000000000601
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34131587; ● Search Scopus @ Elsevier (PMID): 34131587; ● Search Scopus @ Elsevier (DOI): 10.1212/NXG.0000000000000601

(DOI: 10.1212/NXG.0000000000000601, PubMed: 34131587) Hidetada Yamada, Shuichiro Neshige, Takeo Shishido, Hiroki Ueno, Tomohiko Ohshita, Hiroyuki Morino and Hirofumi Maruyama :
Efficacy of Lacosamide in a Patient with Refractory Generalized Epilepsy Based on Video Electroencephalography.,
Internal Medicine, Vol.60, No.22, 3621-3624, 2021.

(要約): A 20-year-old man with drug-resistant generalized epilepsy (GE) was admitted for video electroencephalography (vEEG) monitoring under treatment with multiple antiepileptic drugs, including levetiracetam (3,000 mg/day), valproic acid (800 mg/day), and lacosamide (LCM) (100 mg/day). No seizures were noted after the withdrawal of levetiracetam. However, after the withdrawal of LCM, atypical absence seizures with a 2- to 2.5-Hz generalized spike and wave complex frequently appeared, followed by subsequent generalized-onset tonic-clonic seizures. After re-administration of LCM, the seizures and epileptic discharges clearly disappeared. Subsequent LCM titration was successful in achieving a seizure-free status. Our vEEG results suggest that LCM may be a worthwhile antiepileptic drug adjunct in refractory GE patients without a risk of worsening absence seizures.
(キーワード): Adult / Anticonvulsants / Electroencephalography / Epilepsy, Generalized / Humans / Lacosamide / Male / Seizures / Young Adult
(出版サイトへのリンク): ● Publication site (DOI): 10.2169/internalmedicine.7295-21
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34053987; ● Search Scopus @ Elsevier (PMID): 34053987; ● Search Scopus @ Elsevier (DOI): 10.2169/internalmedicine.7295-21

(DOI: 10.2169/internalmedicine.7295-21, PubMed: 34053987) Tomoyasu Matsubara, Yuishin Izumi, Masaya Oda, Masatoshi Takahashi, Hirofumi Maruyama, Ryosuke Miyamoto, Chigusa Watanabe, Yoshiro Tachiyama, Hiroyuki Morino, Hideshi Kawakami, Yuko Saito and Shigeo Murayama :
An autopsy report of a familial amyotrophic lateral sclerosis case carrying VCP Arg487His mutation with a unique TDP-43 proteinopathy,
Neuropathology, Vol.41, No.2, 118-126, 2021.

(要約): We here report an autopsy case of familial amyotrophic lateral sclerosis (ALS) with p.Arg487His mutation in the valosin-containing protein (VCP) gene (VCP), in which upper motor neurons (UMNs) were predominantly involved. Moreover, our patient developed symptoms of frontotemporal dementia later in life and pathologically exhibited numerous phosphorylated transactivation response DNA-binding protein of 43 kDa (p-TDP-43)-positive neuronal cytoplasmic inclusions and short dystrophic neurites with a few lentiform neuronal intranuclear inclusions, sharing the features of frontotemporal lobar degeneration with TDP-43 pathology type A pattern. A review of previous reports of ALS with VCP mutations suggests that our case is unique in terms of its UMN-predominant lesion pattern and distribution of p-TDP-43 pathology. Thus, this case report effectively expands the clinical and pathological phenotype of ALS in patients with a VCP mutation.
(キーワード): Amyotrophic Lateral Sclerosis / Autopsy / DNA-Binding Proteins / Frontotemporal Lobar Degeneration / Humans / Intranuclear Inclusion Bodies / 男性 (male) / Middle Aged / Motor Neurons / Mutation / TDP-43 Proteinopathies / Valosin Containing Protein
(出版サイトへのリンク): ● Publication site (DOI): 10.1111/neup.12710
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33415820; ● Search Scopus @ Elsevier (PMID): 33415820; ● Search Scopus @ Elsevier (DOI): 10.1111/neup.12710

(DOI: 10.1111/neup.12710, PubMed: 33415820) Hiroyuki Naito, Tomohisa Nezu, Naohisa Hosomi, Daisuke Kuzume, Shiro Aoki, Yuko Morimoto, Takeshi Yoshida, Teppei Kamimura, Yuji Shiga, Naoto Kinoshita, Hiroki Ueno, Hiroyuki Morino and Hirofumi Maruyama :
Increased Serum Alkaline Phosphatase and Functional Outcome in Patients with Acute Ischemic Stroke Presenting a Low Ankle-Brachial Index.,
Journal of Atherosclerosis and Thrombosis, Vol.29, No.5, 719-730, 2021.

(要約): Of the total cohort, 482 patients (22.8%) had a low ABI. ALP levels were higher in patients with a low ABI than in those without (p<0.001). The multivariable logistic analysis revealed that quartiles of ALP levels were significantly associated with a low ABI (odds ratio [OR]: 1.20, 95% confidence interval [CI]: 1.08-1.33). Of the 1322 patients with a premorbid mRS score of 0-2, 434 patients (32.8%) had a poor outcome. The multivariable analysis revealed that elevated serum ALP levels and a low ABI were independently associated with poor stroke outcomes after adjustment for baseline characteristics (OR: 1.21, 95% CI: 1.07-1.38, and OR: 2.00, 95% CI: 1.40-2.84, respectively).
(キーワード): Alkaline Phosphatase / Ankle Brachial Index / Humans / Ischemic Stroke / Predictive Value of Tests / Risk Factors / Stroke
(出版サイトへのリンク): ● Publication site (DOI): 10.5551/jat.62795
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33790143; ● Search Scopus @ Elsevier (PMID): 33790143; ● Search Scopus @ Elsevier (DOI): 10.5551/jat.62795

(DOI: 10.5551/jat.62795, PubMed: 33790143) Y Kanaya, K Kume, Hiroyuki Morino, R Ohsawa, T Kurashige, M Kamada, T Torii, Yuishin Izumi, H Maruyama and H Kawakami :
Analysis of genetic risk factors in Japanese patients with Parkinson's disease,
Journal of Human Genetics, Vol.66, No.10, 957-964, 2021.

(要約): Parkinson's disease (PD) is caused by a combination of genetic and environmental factors. Notably, genetic risk factors vary according to ethnicity and geographical regions, and few studies have analyzed the frequency of PD causative genes in Japanese patients. Therefore, we performed genetic analyses of Japanese patients with PD. We recruited 221 participants, including 26 patients with familial PD. Genetic risk factors were evaluated by target sequencing and gene dosage analysis. We detected the genetic risk factors in 58 cases (26.2%) and classified patients into three groups to clarify the differences in genetic risk factors by age at onset (AAO). The early-onset group (AAO < 50 years) included 18 cases (44.7%), who tended to have a larger number of genetic risk factors than the later-onset groups. Regarding the AAO for each causative gene, patients with PRKN variants were significantly younger at onset than those bearing LRRK2 variants. LRRK2 variants showed similar frequency in each AAO group. Of note, we identified two novel variants. Patients with early-onset PD have more genetic risk factors than patients with late-onset PD. In Japanese patients with PD, PRKN, and LRRK2 were the major PD-related genes. Particularly, LRRK2 was a common genetic factor in all age groups because of the presence of the Asian-specific variant such as LRRK2 p.G2385R. Accumulation of genetic and clinical data can contribute to the development of treatments for PD.
(キーワード): Adult / Age of Onset / Asians / Female / Genetic Predisposition to Disease / Genetic Testing / Genotype / Humans / Leucine-Rich Repeat Serine-Threonine Protein Kinase-2 / Male / Middle Aged / Parkinson Disease / Risk Factors
(出版サイトへのリンク): ● Publication site (DOI): 10.1038/s10038-021-00910-4
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33742109; ● Summary page in Scopus @ Elsevier: 2-s2.0-85102876254

(DOI: 10.1038/s10038-021-00910-4, PubMed: 33742109, Elsevier: Scopus) Shuichiro Neshige, Shiro Aoki, Takeo Shishido, Hiroyuki Morino, Koji Iida and Hirofumi Maruyama :
Socio-economic impact on epilepsy outside of the nation-wide COVID-19 pandemic area.,
Epilepsy & Behavior : E&B, Vol.117, 2021.

(要約): Among the 196 PWE who were evaluated (mean age was 37.8 ± 16.2 years), there were 33 PWE (16.8%) whose seizure frequency had increased after the pandemic began. People with epilepsy with a seizure increase showed a significant association with living alone (p < 0.001), a higher seizure frequency (p < 0.001), negative findings on MRI (p = 0.020), history of dissociative seizure (p < 0.001), mood disorders (p < 0.001), insomnia (p < 0.001), and high psychological stress levels (p = 0.024) at baseline compared with PWE without seizure exacerbation. Multivariate logistic regression analysis revealed that "living alone" (odds ratio (OR) 3.69; 95%CI 1.29-10.52), "high seizure frequency at baseline" (OR 4.53; 95%CI 1.63-12.57), and "comorbidity of insomnia" (OR 9.55; 95%CI 3.71-24.55) were independently associated with seizure exacerbation.
(キーワード): Adult / COVID-19 / Epilepsy / Humans / Middle Aged / Pandemics / SARS-CoV-2 / Socioeconomic Factors / Young Adult
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.yebeh.2021.107886
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33714184; ● Search Scopus @ Elsevier (PMID): 33714184; ● Search Scopus @ Elsevier (DOI): 10.1016/j.yebeh.2021.107886

(DOI: 10.1016/j.yebeh.2021.107886, PubMed: 33714184)

MISC

研究者総覧に該当データはありませんでした。

総説・解説

森野豊之, 丸山博文 :
遺伝性ALSオーバービュー,
Clinical Neuroscience, Vol.41, No.3, 330-333, 2023年3月.

(キーワード): 筋萎縮性側索硬化症 / 原因遺伝子

講演・発表

Yusuke Osaki, Hiroyuki Nodera, Ryosuke Miyamoto, Hiroyuki Morino, M Chan, Ryuji Kaji and Yuishin Izumi :
Peripheral nerve excitability abnormality in spinocerebellar ataxia type 6,
Neuroscience 2023, Nov. 2023. 井上寛章, 行重佐和香, 乾友浩, 笹聡一郎, 青山万理子, 森野豊之, 吉田友紀子, 宮本容子, 今井芳枝, 後藤正和, 滝沢宏光 :
当院乳癌患者におけるBRCA遺伝学的検査の現状,
第30回日本遺伝性腫瘍学会学術集会, 2024年5月. 森野豊之 :
ゲノム情報から診断/治療技術の開発へ,
第11回大学発ベンチャー創出研究会, 2024年2月. 橘このか, 宮本亮介, 武藤浩平, 福本竜也, 山内翔葵, 中森正博, 梶龍兒, 森野豊之, 和泉唯信 :
家族間で異なる表現型を呈したANO3ジストニアの1家系,
第114回日本神経学会中国・四国地方会, 2023年12月. 桑野由紀, NAZERE KEYOUMU, 西田憲生, 森野豊之 :
抗老化RNA uc.138 のm6Aメチル化修飾を介した大腸がん悪性化メカニズム,
第46回日本分子生物学会年会, 2023年12月. 森野豊之 :
ゲノム情報から診断/治療技術の開発へ,
ものづくり未来共創機構シンポジウム2023, 2023年12月. 森野豊之 :
ゲノム医療の進歩と徳島大学病院の取り組み,
2023年度第9回徳島市医師会学術講演会, 2023年12月. 山田英忠, 山崎雄, 竹林佳子, 矢澤恭介, 笹西美和子, 元田敦子, 中森正博, 森野豊之, 高橋哲也, 丸山博文 :
加熱式タバコのエアロゾル吸入がアルツハイマー病マウスモデル中枢神経系に及ぼす影響,
第42回日本認知症学会学術集会, 2023年11月. 森野豊之 :
ゲノム技術の進歩と小児診療におけるゲノム医療,
第159回日本小児科学会徳島地方会学術集会, 2023年6月. 行重佐和香, 井上寛章, 乾友浩, 笹聡一郎, 青山万理子, 奥村和正, 森野豊之, 吉田友紀子, 宮本容子, 滝沢宏光 :
BRCA遺伝学的検査の結果inconclusiveとなった3例,
第29回日本遺伝性腫瘍学会学術集会, 2023年6月. 山内翔葵, 宮本亮介, 武藤浩平, 桑野由紀, NAZERE KEYOUMU, 西田憲生, 橘このか, 和泉唯信, 森野豊之 :
表現型に基づく優先順位付けを用いたALSの病的バリアント検索,
第64回日本神経学会学術大会, 2023年6月. 橘このか, Ryosuke Miyamoto, Hiroyuki Morino, 福本竜也, 松本真一, 目崎高広, 星野恭子, Koutaro Asanuma, Takashi Sakamoto, Ryuji Kaji, Yuishin Izumi and Consortium Dystonia Japan :
Genetical and clinical features in a cohort of Japanese patients with dystonia,
第64回日本神経学会学術大会, May 2023. 森野豊之 :
徳島大学病院のゲノム医療センターについて,
難病医療講演会プログラムIRUD, 2023年1月. Aya Gohji, Hiroyuki Morino, Asami Okada, Tatsuo Mori, Ken-ichi Suga, Yumiko Kotani, 瀬山理惠, 内山由理 and 松本直通 :
Coffin-siris syndrome with persistent open anterior fontanelle in a boy arising from a novel de novo ARID2 variant,
日本人類遺伝学会第67回大会, Dec. 2022. 花田健太, 大崎裕亮, 宮本亮介, 土師正太郎, 森野豊之, 和泉唯信 :
新規のMORC2変異を認めたCharcot-Marie-Tooth病2Z型の1例,
第112回日本神経学会中国・四国地方会, 2022年12月. 花田健太, 大崎裕亮, 宮本亮介, 土師正太郎, 森野豊之, 和泉唯信 :
MORC2新規変異を認めたCharcot-Marie-Tooth病2Z型の1例,
第33回日本末梢神経学会学術集会, 2022年9月. 倉重毅志, 森野豊之, 村尾智美, 和泉唯信, 杉浦智仁, 倉岡和矢, 川上秀史, 鳥居剛, 丸山博文 :
ALS患者の筋内神経束でのTDP-43凝集,
第8回日本筋学会学術集会, 2022年8月. 武藤浩平, 宮本亮介, 沖良祐, 宮﨑由道, 藤井大樹, 二宮伸介, 秋山倫之, 梶龍兒, 森野豊之, 和泉唯信 :
Geniospasm4,
第63回日本神経学会学術大会, 2022年5月. 武藤浩平, 宮本亮介, 沖良祐, 宮﨑由道, 藤井大樹, 二宮伸介, 秋山倫之, 梶龍兒, 森野豊之, 和泉唯信 :
本邦におけるGeniospasmの4家系,
第63回日本神経学会学術大会, 2022年5月. 大崎裕亮, 宮本亮介, 森野豊之, 和泉唯信 :
Distal hereditary motor neuropathyを呈したMARS新規変異を有する1家系,
第63回日本神経学会学術大会, 2022年5月. 桑野由紀, 西田憲生, 森野豊之 :
RNA修飾を介した大腸がん細胞の抗老化スイッチの解明,
第44回日本分子生物学会年会, 2021年12月. 森野豊之 :
脊髄小脳変性症42型の原因と新規治療戦略,
徳島県市民公開講座難病医療講演会, 2021年10月. Takashi Kurashige, Hiroyuki Morino, Hiroki Ueno, Tomomi Murao, Tomoaki Watanabe, Takao Hinoi, Ichizo Nishino, Tsuyoshi Torii and Hirofumi Maruyama :
Gastrointestinal cancer occurs as extramuscular manifestation in FSHD1 patients,
日本人類遺伝学会第66回大会, Oct. 2021. 原直之, Hiroyuki Morino, 松田由喜子, 佐藤健一, 橋本浩一, 丸山博文 and 川上秀史 :
Zonisamide can ameliorate the conduction of the mutant CaV3.1 that causes spinocerebellar ataxia,
第62回日本神経学会学術大会, May 2021. 松田由喜子, Hiroyuki Morino, 外丸祐介, 倉重毅志, 丸山博文 and 川上秀史 :
Transcriptomic analysis using model mice of spinocerebellar ataxia 42,
第62回日本神経学会学術大会, May 2021.

研究会・報告書: 森野豊之 :
神経筋疾患とゲノム情報,
第15回脳科学クラスターミニリトリート, 2024年2月. 坂原英皓, 内藤裕之, 頼近恭典, 田妻卓, 中森正博, 青木志郎, 山崎雄, 森野豊之, 高橋哲也, 丸山博文 :
濃厚な家族歴を有し，パーキンソニズムを呈した50歳女性例,
第53回症例から学ぶ脳神経内科in広島, 2024年2月. 森野豊之 :
遺伝性神経疾患に対する遺伝カウンセリング,
遺伝性ATTRアミロイドーシスセミナー in 徳島, 2024年2月. 森野豊之 :
神経変性疾患の遺伝学的解析,
Fukuoka Neurology Research Forum, 2023年9月. 森野豊之 :
ゲノム技術の進歩と今後の医学,
2022遺伝・発生・再生クラスターミニリトリート, 2022年12月. 森野豊之 :
遺伝的要因から考えるパーキンソン病の発症機序と治療戦略,
第42回症例から学ぶ神経内科 in 広島, 2022年2月.

特許: 研究者総覧に該当データはありませんでした。
作品: 研究者総覧に該当データはありませんでした。
補助金・競争的資金: パーキンソン病におけるα-シヌクレイン凝集機序の解明と新規治療への応用 (研究課題/領域番号: 23K06828 )
Necroptosisを介したALSの運動神経変性の病態機序と新規治療の探索 (研究課題/領域番号: 23H02827 )
新規ミトコンドリア蛋白質の構造異常によるALS病態の解析と評価モデル系の開発 (研究課題/領域番号: 22H02950 )
脊髄小脳変性症モデルマウスを用いたCRISPR/Cas13による新しい核酸医療 (研究課題/領域番号: 19K07994 )
ヒト一倍体細胞を用いた遺伝子トラップ法によるTDP-43関連遺伝子の同定 (研究課題/領域番号: 16K15481 )
iPS細胞を用いたミトコンドリアDNA維持機構の破綻と神経変性への関与 (研究課題/領域番号: 15K15083 )
遺伝学的アプローチによる小脳機能障害の解明 (研究課題/領域番号: 26242085 )
ＡＬＳにおけるＯｐｔｉｎｅｕｒｉｎの神経細胞毒性に関する分子メカニズムの解明 (研究課題/領域番号: 23591246 )
常染色体劣性脊髄小脳変性症の新規遺伝子 (研究課題/領域番号: 19390241 )
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2024年5月15日更新

専門分野・研究分野: 遺伝学 (Genetics)
所属学会・所属協会: 日本神経学会
日本老年医学会
委員歴・役員歴: 日本神経学会 (代議員 [2021年5月〜2022年3月])
日本老年医学会 (代議員 [2018年7月〜2022年3月])
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Jグローバル最終確認日: 2024/5/11 01:29
氏名（漢字）: 森野豊之
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氏名（英字）: Morino Hiroyuki
所属機関: 徳島大学大学院教授

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researchmap最終確認日: 2024/5/12 04:04
氏名（漢字）: 森野豊之
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氏名（英字）: Morino Hiroyuki
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所属: 徳島大学大学院
部署: 医歯薬学研究部遺伝情報医学分野
職名: 教授
学位: 博士（医学）
学位授与機関: 広島大学
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2024年5月11日更新

研究者番号: 10397953

所属（現在）: 2024/4/1 : 徳島大学, 大学院医歯薬学研究部(医学域), 教授

所属（過去の研究課題 情報に基づく）*注記: 2021/4/1 – 2023/4/1 : 徳島大学, 大学院医歯薬学研究部(医学域), 教授
2015/4/1 – 2017/4/1 : 広島大学, 原爆放射線医科学研究所, 准教授
2011/4/1 – 2013/4/1 : 広島大学, 原爆放射線医科学研究所, 助教
2007/4/1 – 2009/4/1 : 広島大学, 原爆放射線医科学研究所, 助教

審査区分/研究分野

研究代表者

生物系 / 医歯薬学 / 内科系臨床医学 / 神経内科学
生物系 / 医歯薬学 / 基礎医学 / 病態医化学
小区分51030:病態神経科学関連

研究代表者以外

生物系 / 医歯薬学 / 内科系臨床医学 / 神経内科学
総合系 / 複合領域 / 脳科学 / 基盤・社会脳科学
小区分52020:神経内科学関連
小区分51030:病態神経科学関連

キーワード

研究代表者

神経分子病態 / 筋萎縮性側索硬化症 / 神経分子病態学 / 遺伝子 / 脳神経疾患 / ミトコンドリア / パーキンソン病 / α-シヌクレイン / 凝集体形成 / ライソソーム

研究代表者以外

臨床神経分子遺伝学 / 脊髄小脳変性症 / 劣性遺伝 / SNP / 脳神経疾患 / ゲノム解析 / 遺伝学 / Ca チャンネル / 遺伝子 / 神経科学 / 遺伝性脊髄小脳変性症 / TDP-43 / 筋萎縮性側索硬化症 / プルキンエ細胞 / CACNA1G / FUS / DHX30 / RNA / 低分子スクリーニング / Fused in sarcoma (FUS) / 変異遺伝子スクリーニング / necroptosis

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2024年4月30日

エピトランスクリプトームを応用した新規創薬技術の開発

NAZERE KEYOUMU 桑野由紀森野豊之

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