Details of a Researcher - SHIMOHAMA Shiyun

Latitude and HLA-DRB1 alleles independently affect the emergence of cerebrospinal fluid IgG abnormality in multiple sclerosis

Masaaki Niino, Shinya Sato, Toshiyuki Fukazawa, Satoshi Yoshimura, Shin Hisahara, Takuya Matsushita, Noriko Isobe, Kazuto Yoshida, Hideki Houzen, Yusei Miyazaki, Shun Shimohama, Seiji Kikuchi, Jun-ichi Kira

MULTIPLE SCLEROSIS JOURNAL ( SAGE PUBLICATIONS LTD ) 21 ( 9 ) 1112 - 1120 2015.08 [Refereed]

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Background: It is unclear whether the prevalence of oligoclonal IgG bands (OCBs) in multiple sclerosis (MS) is different between northern and southern regions of Asia. Objective: This study aimed to compare the prevalence of OCBs and positive cerebrospinal fluid (CSF) findings between northern and southern regions of Japan and to investigate the association of these CSF findings with HLA-DRB1 alleles. Methods: The study included 180 MS patients from Hokkaido (northern Japan) and 184 patients from Kyushu (southern Japan). The IgG index was defined as increased if it was >0.658. Presence of CSF OCBs and/or increased IgG index was defined as positive CSF findings. Results: Positive CSF findings and OCB positivity were significantly higher in MS patients from Hokkaido than in those from Kyushu (p < 0.0001 for both). Logistic regression analysis revealed that after adjusting for covariates that can be related to abnormal CSF IgG production, the geographic region (Hokkaido) showed odds ratios (ORs) of 4.08 and 2.57, whereas the HLA-DRB1*04:05 allele showed ORs of 0.36 and 0.30 for positive CSF findings and OCB positivity, respectively. Conclusions: The results indicate that latitude and HLA-DRB1 alleles independently affect the emergence of CSF IgG abnormalities in Japanese patients with MS.

DOI PubMed
Intravenous mesenchymal stem cell administration exhibits therapeutic effects against 6-hydroxydopamine-induced dopaminergic neurodegeneration and glial activation in rats

Syuuichirou Suzuki, Jun Kawamata, Naoyuki Iwahara, Akihiro Matsumura, Shin Hisahara, Takashi Matsushita, Masanori Sasaki, Osamu Honmou, Shun Shimohama

NEUROSCIENCE LETTERS ( ELSEVIER IRELAND LTD ) 584 276 - 281 2015.01 [Refereed]

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To explore a novel therapy against Parkinson's disease (PD), we evaluated the therapeutic effects of human bone marrow-derived mesenchymal stem cells (hBM-MSCs), pluripotent stromal cells with secretory potential of various neurotrophic and anti-inflammatory factors, in a hemi-parkinsonian rat model. The unilateral intrastriatal 6-hydroxydopamine (6-OHDA)-lesioned rats were injected hBM-MSCs (1.0 x 10(7) cells) or PBS intravenously 16 days after lesioning. Administration of hBM-MSCs inhibited methamphetamine-stimulated rotational behavior at 7, 14, 21 and 28 days after transplantation. Immunohistochemical analysis also showed that number of TH-positive neurons in the substantia nigra pars compacta was significantly preserved in hBM-MSCs-transplanted rats compared to sham-operated rats, whereas the immunoreactivity of ionized calcium binding adaptor molecule 1 was markedly inhibited. In this study, we demonstrated the therapeutic effects of intravenous hBM-MSCs administration in parkinsonian model rats presenting distinct parkinsonian phenotype at 16 days after 6-OHDA lesioning. The favorable findings raise the possibility that hBM-MSCs could be a novel therapeutic option to promote survival of dopaminergic neurons in PD. (C) 2014 Elsevier Ireland Ltd. All rights reserved.

DOI PubMed
Idiopathic Normal Pressure Hydrocephalus has a Different Cerebrospinal Fluid Biomarker Profile from Alzheimer's Disease

Naoto Jingami, Megumi Asada-Utsugi, Kengo Uemura, Rio Noto, Makio Takahashi, Akihiko Ozaki, Takeshi Kihara, Takashi Kageyama, Ryosuke Takahashi, Shun Shimohama, Ayae Kinoshita

JOURNAL OF ALZHEIMERS DISEASE ( IOS PRESS ) 45 ( 1 ) 109 - 115 2015 [Refereed]

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The diagnosis of idiopathic normal pressure hydrocephalus (iNPH) is sometimes complicated by concomitant Alzheimer's disease (AD) pathology. The purpose of the present study is to identify an iNPH-specific cerebrospinal fluid (CSF) biomarker dynamics and to assess its ability to differentiate iNPH from AD. Total tau (t-tau), tau phosphorylated at threonine 181 (p-tau), amyloid-beta (A beta) 42 and 40, and leucine-rich alpha-2-glycoprotein (LRG) were measured in 93 consecutive CSF samples consisting of 55 iNPH (46 tap test responders), 20 AD, 11 corticobasal syndrome, and 7 spinocerebeller disease. Levels of t-tau and p-tau were significantly decreased in iNPH patients especially in tap test responders compared to AD. Correlation was observed between Mini-Mental State Examination scores and A beta(42) in AD (R = 0.44) and mildly in iNPH (R = 0.28). Although A beta(42/40) ratio showed no significant difference between iNPH and AD (p = 0.08), the levels of A beta(40) and A beta(42) correlated positively with each other in iNPH (R = 0.73) but much less in AD (R = 0.26), suggesting that they have discrete amyloid clearance and pathology. LRG levels did not differ between the two. Thus, our study shows that although CSF biomarkers of iNPH patients can be affected by concomitant tau and/or amyloid pathology, CSF t-tau and p-tau are highly useful for differentiation of iNPH and AD.

DOI PubMed
Temporal Changes of CD68 and alpha 7 Nicotinic Acetylcholine Receptor Expression in Microglia in Alzheimer's Disease-Like Mouse Models

Akihiro Matsumura, Syuuichirou Suzuki, Naotoshi Iwahara, Shin Hisahara, Jun Kawamata, Hiromi Suzuki, Ayano Yamauchi, Kazuyuki Takata, Yoshihisa Kitamura, Shun Shimohama

JOURNAL OF ALZHEIMERS DISEASE ( IOS PRESS ) 44 ( 2 ) 409 - 423 2015 [Refereed]

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We previously reported that activated microglia are involved in amyloid-beta (A beta) clearance and that stimulation of alpha 7 nicotinic acetylcholine receptors ( nAChR) in microglia enhances A beta clearance. Nevertheless, how microglia and alpha 7 nAChR in microglia are affected in Alzheimer's disease ( AD) remains unknown. The present study aimed to collect fundamental data for considering whether microglia are potential targets for AD treatment and the appropriate timing of therapeutic intervention, by evaluating the temporal changes of A beta, microglia, neurons, presynapses, and alpha 7 nAChR by immunohistochemical studies in mouse models of AD. In an A beta-injected AD mouse model, we observed early accumulation of CD68-positive microglia at A beta deposition sites and gradual reduction of A beta. Microglia were closely associated with A beta deposits, and were confirmed to participate in clearing A beta. In a transgenic mouse model of AD, we observed an increase in A beta deposition from 6 months of age, followed by a gradual increase in microglial accumulation at A beta deposit sites. Activated microglia in APdE9 mice showed two-step transition: a CD68-negative activated form at 6-9 months and a CD68-positive form from 12 months of age. In addition, alpha 7 nAChR in microglia increased markedly at 6 months of age when activated microglia appeared for the first time, and decreased gradually coinciding with the increase of A beta deposition. These findings suggest that early microglial activation is associated with alpha 7 nAChR upregulation in microglia in APdE9 mice. These novel findings are important for the development of new therapeutic strategy for AD.

DOI PubMed
Long-term clinical and radiological improvement of chronic acquired hepatocerebral degeneration after obliteration of portosystemic shunt: Report of a case

Shin Hisahara, Takashi Matsushita, Mizuki Kitamura, Shinichi Mezawa, Michio Nonaka, Tomihiro Imai, Shun Shimohama

JOURNAL OF THE NEUROLOGICAL SCIENCES ( ELSEVIER SCIENCE BV ) 346 ( 1-2 ) 303 - 306 2014.11 [Refereed]

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Neurological manifestations are common in patients with decompensated cirrhosis. The majority of these patients show hepatic encephalopathy or chronic acquired (non-Wilsonian) hepatocerebral degeneration (CAHD). They characteristically present with dysarthria, ataxia, involuntary movements, and altered mental status. Neuroradiological examination in patients with hepatic encephalopathy often shows abnormal signals in multiple regions of the brain, such as the pallidum, putamen, caudate nucleus, hemispheric white matter, and ventral midbrain. The pathogenesis of hepatic encephalopathy and CAHD is poorly understood and the response to conventional therapies is often poor. We report a male patient with cirrhosis of unknown cause, who developed slowly progressive cerebellar truncal and limb ataxia and slurred speech. Magnetic resonance imaging (MRI) showed focal T2 hyperintensity in bilateral dentate nuclei and middle cerebellar peduncles (MCPs). After treatment by obliteration of the portosystemic shunt, clinical manifestations and MM abnormalities were dramatically improved. He was followed for six years until he died of uncontrollable bleeding due to hepatocellular carcinoma. At the last examination 9 months before death, he showed no apparent aggravation of neurological symptoms, and no abnormal signal intensities in the MCPs and supratentorial compartment. The clinical course and changes of brain MM findings of this case are extremely rare, suggesting that obliteration of the portosystemic shunt may be effective for CAHD over long term. (C) 2014 Elsevier B.V. All rights reserved.

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Nicotinic receptor stimulation protects neurons against glutamate-and β-amyloid-induced cytotoxicity

In"Alzheimer's Disease and Related Disorders : Etiology, Pathagenesis and therapeutitics"John Wiley & Sons, Ltd. 1999
Intracerebral grafting of genetically modified cells : application to a rat model of Parkinson's disease

Raven Press, "Advances in Neurology" 1993

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Misc 【 display / non-display 】

High mobility group box protein-1 inhibits microglial A beta clearance and enhances A beta neurotoxicity

K Takata, Y Kitamura, D Tsuchiya, T Kawasaki, T Taniguchi, S Shimohama

JOURNAL OF NEUROSCIENCE RESEARCH ( WILEY-LISS ) 78 ( 6 ) 880 - 891 2004.12

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One pathogenic characteristic of Alzheimer's disease (AD) is the formation of extracellular senile plaques with accumulated microglia. According to the amyloid hypothesis, the increase or accumulation of amyloid-beta (Abeta) peptides in the brain parenchyma is the primary event that influences AD pathology. Although the role of microglia in AD pathology has not been clarified, their involvement in Abeta clearance has been noted. High mobility group box protein-1 (HMGB1) is an abundant nonhistone chromosomal protein. We reported recently that HMGB1 was associated with senile plaques and the total protein level significantly increased in AD brain. In this study, diffuse HMGB1 immunoreactivity was observed around dying neurons in the kainic acid- and Abeta1-42 (Abeta42)injected rat hippocampi. HMGB1 also colocalized with Abeta in the Abeta42-injected rats but not in transgenic mice, which show massive Abeta production without neuronal loss in their brains. Furthermore, coinjection of HMGB1 delayed the clearance of Abeta42 and accelerated neurodegeneration in Abeta42-injected rats. These results suggest that HMGB1 released from dying neurons may inhibit microglial Abeta42 clearance and enhance the neurotoxicity of Abeta42. HMGB1 may thus be another target in the investigation of a therapeutic strategy for AD. (C) 2004 Wiley-Liss, Inc.

DOI
Galantamine modulates nicotinic receptor and blocks A beta-enhanced glutamate toxicity

T Kihara, H Sawada, T Nakamizo, R Kanki, H Yamashita, A Maelicke, S Shimohama

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS ( ACADEMIC PRESS INC ELSEVIER SCIENCE ) 325 ( 3 ) 976 - 982 2004.12

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Galantamine is a plant alkaloid that is used in the treatment of Alzheimer's disease. We have studied the effects of galantamine on beta-amyloid-enhanced glutamate toxicity using primary rat cultured cortical neurons. Nicotine and galantamine alone, and in combination, protected neurons against this neurotoxicity. The protection was not blocked by alpha4beta2 nicotinic acetylcholine receptor (nAChR) antagonists, but was partially blocked by 0 nAChR antagonists. Galantamine induced phosphorylation of Akt, an effector of phosphatidylinositol 3-kinase (PI3K), while PI3K inhibitors blocked the protective effect and Akt phosphorylation. The antibody FK1, which selectively blocks the allosterically potentiating ligand site on nAChR, significantly reduced the galantamine-induced protection and Akt phosphorylation. Furthermore, suppression of 0 nAChR using an RNA interference technique reduced Akt phosphorylation induced by galantamine. Our data suggest that neuroprotection by galantamine is mediated, at least in part, by alpha7 nAChR-PI3K cascade. (C) 2004 Elsevier Inc. All rights reserved.

DOI
A new form of congenital proprioceptive sensory neuropathy associated with arthrogryposis multiplex

H Shibasaki, T Hitomi, T Mezaki, T Kihara, H Tomimoto, A Ikeda, S Shimohama, M Ito, N Oka

JOURNAL OF NEUROLOGY ( DR DIETRICH STEINKOPFF VERLAG ) 251 ( 11 ) 1340 - 1344 2004.11

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We report two siblings who presented with non-progressive marked sensory ataxia associated with arthrogryposis multiplex congenita (AMC). Deep tendon reflexes and H reflex were completely absent, but F waves were preserved. The sensory nerve conduction studies indicated the presence of relatively mild sensory polyneuropathy. The conventional somatosensory evoked potentials (SEPs) showed mildly prolonged latency for both the peripheral and cortical responses, suggesting a slowed conduction through the peripheral as well as central pathway. However, the 'proprioceptive SEPs' were absent, in conformity with complete loss of joint sense. Sural nerve biopsy revealed only mild thinning of myelin in the younger sister but was entirely normal in her brother. Taken together with the characteristic electrophysiological findings, the symptoms were considered to be due to predominant involvement of a selective population of somatosensory ganglions. The present cases showed no progression of the neurological deficit what-so-ever since birth, which strongly suggests a developmental anomaly or aplasia of a limited population of peripheral sensory neurons.

DOI
Differential expression profiles of PLC-beta 1 and -delta 1 in primary cultured rat cortical neurons treated with N-methyl-D-aspartate and peroxynitrite

K Nagasawa, K Nishida, K Nagai, S Shimohama, S Fujimoto

NEUROSCIENCE LETTERS ( ELSEVIER SCI IRELAND LTD ) 367 ( 2 ) 246 - 249 2004.09

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Phospholipase C (PLC)-delta1 protein appears to accumulate aberrantly in Alzheimer's disease brains and its expression is reported to be induced by overstimulation of N-methyl-D-aspartate (NMDA) receptor, but there is little knowledge on its physiological role. To clarify this, we examined the expression profile of PLC-delta1 in primary cultured rat cortical neurons treated with NMDA or peroxynitrite, in comparison with those of PLC-delta1 and -gamma1, the overexpression of both of which protects cells from oxidative stress. Overstimulation of NMDA receptor decreased and increased the expression of PLC-beta1 and -delta1, respectively, but did not affect that of PLC-gamma1, in the neurons. The viability of neurons decreased depending on the period of treatment with S-nitroso-N-acetyl D,L-penicillamine (SNAP), there being a significant decrease on 9 h treatment. On examination of the expression profiles of PLC isozymes after treatment of neurons with SNAP, PLC-P I was found to be increased after 1 h treatment and decreased after 9 h treatment, while PLC-delta1 was significantly increased, especially after 5 h treatment. Peroxynitrite treatment caused a dose-dependent decrease in the viability of neurons, and expression of PLC-beta1 was increased by a nontoxic level of peroxynitrite and decreased by a toxic level of it, while that of PLC-delta1 was increased by a sublethal level of it. These findings suggested that induction of PLC-beta1 might protect neurons from oxidative stress, but that of PLC-delta1 might have the opposite role, although both isozymes responded to oxidative stress. (C) 2004 Published by Elsevier Ireland Ltd.

DOI
Effects of mitochondrial dysfunction on glutamate receptor-mediated neurotoxicity in cultured rat spinal motor neurons

R Kanki, T Nakamizo, H Yamashita, T Kihara, H Sawada, K Uemura, J Kawamata, H Shibasaki, A Akaike, S Shimohama

BRAIN RESEARCH ( ELSEVIER SCIENCE BV ) 1015 ( 1-2 ) 73 - 81 2004.07

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Glutamate-induced excitotoxicity is implicated as playing a key role in the pathogenesis of amyotrophic lateral sclerosis (ALS), and mitochondrial dysfunction is also found in ALS patients. We investigated the relationship between glutamate excitotoxicity and mitochondrial dysfunction elicited by rotenone (a complex I inhibitor), malonate (a complex II inhibitor), or antimycin (a complex III inhibitor), in primary cultures of the embryonic rat spinal cord. Rotenone and malonate induced relatively selective toxicity against motor neurons as compared to non-motor neurons, whereas antimycin caused non-selective toxicity. The toxicity of rotenone was prevented by a non-N-methyl-D-aspartate (NMDA) receptor antagonist, 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) but not by an NMDA receptor antagonist, 5-methyl-10, 11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine hydrogen maleate (MK-801). The toxicity of malonate was blocked by both CNQX and MK-801. The toxicity of antimycin was affected by neither CNQX nor MK-801. When mitochondrial complex I was mildly inhibited by a sub-lethal concentration of rotenone, AMPA-induced motor neuron death was significantly exacerbated. A sub-lethal concentration of malonate exacerbated both NMDA- and AMPA-induced motor neuron death. These data suggest that mitochondrial dysfunction predisposes motor neurons to ionotropic glutamate receptor-mediated excitotoxicity. (C) 2004 Elsevier B.V. All rights reserved.

DOI

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パーキンソン病診断キットおよびパーキンソン病診断方法

澤田秀幸, 下濱俊

Patent

J-GLOBAL
アルツハイマー病のタンパク質分子レベルにおける検出方法

下濱俊, 辻輝之

Patent

J-GLOBAL
脳アミロイドーシス予防・治療薬のスクリーニング方法

特許第4242128号

下濱俊, 谷口隆之, 北村佳久

Patent

J-GLOBAL
パーキンソン病診断キットおよびパーキンソン病診断方法

Patent

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2003-405942
脳アミノロイドーシス予防・治療薬のスクリーニング方法

Patent

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2002-272195号

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Works 【 display / non-display 】

アルツハイマー病におけるプロテオーム解析

2001

　

　
Proteome analysis in Alzheimer's disease

2001

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Awards 【 display / non-display 】

公益信託加藤記念難病研究助成賞受賞

1995
日本医師会医学研究助成費受賞

1994
財団法人サンド老化および老年医学研究基金研究助成賞受賞

1992

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Research Projects 【 display / non-display 】

The method of "pre and post " graduate medical education that correct regional disparity

Grant-in-Aid for Scientific Research (C)

Project Year :

2011

-

2013

MASAKI Saitoh, SHIMOHAMA Shun, HOUKIN Kiyohiro

Authorship： Collaborating Investigator(s) (not designated on Grant-in-Aid)

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We showed that care staff in local cities have few opportunities to get various medical information. Although their knowledge of stroke is not enough,they want to get additional information of stroke, first-aid procedure in medical emergency, and management of dementia. We developed educational system about medical emergency for stroke and dementia care staff. Particularly, in Akabira city, Hokkaido, we performed the education about stroke, TIA, and medical emergency to 56% of care staff in Akabira city during one year. We published two text books on these findings.
Pathophysiological analysis for the ischemic brain damage using in vitro blood-brain barrier system

Grant-in-Aid for Challenging Exploratory Research

Project Year :

2011

-

2012

SHIMOHAMA Shun, MINAMI Masabumi

Authorship： Principal investigator

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To study transmigration of mesenchymal stem cells (MSCs) across the blood-brain barrier (BBB), we developed an in vitro BBB system consisting of rat brain microvascular endothelial cells (BMECs). Time-lapse imaging using this system revealed that MSCs transmigrated across the BMEC monolayer through transiently formed intercellular gaps between the BMECs. In addition, we developed an in vitro imaging system for simultaneous analysis in real time between claudin-5, a tight junction protein, and intracellular calcium dynamics in BMECs during MSC transmigration.
Basic reserach for developing a new therapy by transplantation of mesenchymal stem cells against neurodegenerative diseases

Grant-in-Aid for Scientific Research (B)

Project Year :

2010

-

2013

SHIMOHAMA Shun, HONMOU Osamu

Authorship： Principal investigator

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To explore a novel therapy against Parkinson disease, we evaluated the therapeutic effects of human bone marrow-derived mesenchymal stem cells (hBM-MSCs) in 6-OHDA induced Parkinson disease model rats. Intravenous administration of hBM-MSCs inhibited methamphetamine-stimulated rotational behevior at 7, 14, 21 and 28 days after transplantation. Rats injected with hBM-MSCs displayed significant preservation of tyrosine hydroxylase (TH)-positive fibers in the striatum and the number of TH-positive neurons in the substantia nigra compacta (SNpc). In contrast, the immunoreactivity of ionized calcium binding adaptor molecule 1 (Iba1) was markedly inhibited by intravenous admnistration of hBM-MSCs. The findings that hBM-MSCs attenuate 6-OHDA-induced dopaminergic neurodegeneration and glial activation raise the possibility that hBM-MSCs could be a novel therapeutic option to prevent Parkinson disease development.
Functional analysis of histone deacetylase SIRT in the pathophysiology of neurodegenerative disorders

基盤研究(C)

Project Year :

2009

-

2011

Shin HISAHARA, Shun SHIMOHAMA

Authorship： Collaborating Investigator(s) (not designated on Grant-in-Aid)

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We now have investigating the function of histone deacetylase SIRT(sirtuin). To explore preventive effect against cell death, we have performed cell viability assay in PC12 and SHSY5Y cells with administration of hydrogen peroxide(H2O2) and 6-hydroxydopamine(6-OHDA). Administration of resveratrol, an activator of SIRT, and overexpression of SIRT1 resulted in significant inhibition of oxidative stress-induced cell death. We also found that overexpression of SIRT1H355Y, a dominant-negative SIRT1, showed partial inhibition of cell death. These results indicate that SIRT1 promotes cellular viability via deacetylase activity-dependent and -independent mechanisms.
筋萎縮性側索硬化症治療薬としての分子シャペロン誘導剤の探索研究

萌芽研究

Project Year :

2005

-

2006

下濱俊, 川又純

Authorship： Principal investigator

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家族性筋萎縮性側索硬化症(FALS)の原因遺伝子である変異SOD1の病態的意義を解明するために、変異SOD1と結合する新たなタンパク質を同定し、その役割について解析した。マウスのneuroblastoma cell lineであるNeuro2Aに変異SOD1(G93A)を過剰発現したサンプルおよび変異SOD1(G93A)トランスジェニックマウスの脊髄組織で変異SOD1と特異的に結合するバンドが認められ、質量分析にてheatshock protein 105(HSP105)と判明した。HSP105と変異SOD1の結合は抗体を用いたプロットでも確認した。また一定量の沈降抗体により共沈するHSP105の量は、wild type SOD1では認められず、変異SOD1の病原性の強さと相関していることが分かった。G93Aトランスジェニックマウス脊髄の主要なシャペロンのタンパク量の経時的な変化を検討したところ、運動麻痺の進行期においてHSP70およびHSP27は上昇を示したが、対照的にHSP105は減少を示した。野生型マウスの脊髄前角の免疫染色では、SMI32で染色される運動ニューロンはHSP105で染色され、HSP105は運動ニューロンに多いことが判明した。さらに、培養細胞系でHSP105の過剰発現により変異SOD1を含む凝集体の形成が抑制されることが判明した。以上の結果は、HSP105は変異SOD1と結合し、変異SOD1の凝集形成を抑制することを示した。神経難病であるALSの新たな治療法として、HSP105レベルを増加させる手法の可能性を示唆していると考えられる。

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