研究者詳細 - 山下　徹

論文 - 山下　徹

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GPIHBP1 autoantibody syndrome during interferon beta 1a treatment

Jun Eguchi, Kazuya Miyashita, Isamu Fukamachi, Katsuyuki Nakajima, Masami Murakami, Yuko Kawahara, Toru Yamashita, Yasuyuki Ohta, Koji Abe, Atsuko Nakatsuka, Mai Mino, Satoru Takase, Hiroaki Okazaki, Robert A. Hegele, Michael Ploug, Xuchen Hu, Jun Wada, Stephen G. Young, Anne P. Beigneux

JOURNAL OF CLINICAL LIPIDOLOGY 13 ( 1 ) 62 - 69 2019年2月

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

BACKGROUND: Autoantibodies against glycosylphosphatidylinositol-anchored high-density lipoprotein-binding protein 1 (GPIHBP1) cause chylomicronemia by blocking the ability of GPIHBP1 to bind lipoprotein lipase (LPL) and transport the enzyme to its site of action in the capillary lumen.OBJECTIVE: A patient with multiple sclerosis developed chylomicronemia during interferon (IFN) beta 1a therapy. The chylomicronemia resolved when the IFN beta 1a therapy was discontinued. Here, we sought to determine whether the drug-induced chylomicronemia was caused by GPIHBP1 autoantibodies.METHODS: We tested plasma samples collected during and after IFN beta 1a therapy for GPIHBP1 autoantibodies (by western blotting and with enzyme-linked immunosorbent assays). We also tested whether the patient's plasma blocked the binding of LPL to GPIHBP1 on GPIHBP1-expressing cells.RESULTS: During IFN beta 1a therapy, the plasma contained GPIHBP1 autoantibodies, and those autoantibodies blocked GPIHBP1's ability to bind LPL. Thus, the chylomicronemia was because of the GPIHBP1 autoantibody syndrome. Consistent with that diagnosis, the plasma levels of GPIHBP1 and LPL were very low. After IFN beta 1a therapy was stopped, the plasma triglyceride levels returned to normal, and GPIHBPI autoantibodies were undetectable.CONCLUSION: The appearance of GPIHBP1 autoantibodies during IFN Pla therapy caused chylomicronemia. The GPIHBP1 autoantibodies disappeared when the IFN beta 1a therapy was stopped, and the plasma triglyceride levels fell within the normal range. (C) 2018 National Lipid Association. All rights reserved.

DOI： 10.1016/j.jacl.2018.10.004

Asymmetrical and Isolated Hypoglossal Nerve Palsy Accompanied by a New Subset of Anti-ganglioside Antibodies in a Patient with Diffuse Large B Cell Lymphoma. 査読

Yasuyuki Ohta, Yuko Kawahara, Koh Tadokoro, Kota Sato, Ryo Sasaki, Yoshiaki Takahashi, Mami Takemoto, Nozomi Hishikawa, Toru Yamashita, Takeru Asano, Tomoko Inomata, Koji Abe

Internal medicine (Tokyo, Japan) 58 ( 2 ) 283 - 286 2019年1月

記述言語：英語掲載種別：研究論文（学術雑誌）

Malignant lymphoma sometimes involves peripheral nerves due to paraneoplastic syndrome associated with anti-ganglioside antibodies. We report a very rare case of malignant lymphoma accompanied by an asymmetrical and isolated hypoglossal nerve palsy associated with a new subset of anti-ganglioside antibodies. Magnetic resonance imaging and 18F-2-deoxy-2-fluoro-D-glucose position emission tomography showed no abnormalities of the hypoglossal nerve nucleus; however, the patient' s serum was positive for anti-sulfated glucuronyl paragloboside IgM antibodies as well as anti-GM1 IgM and anti-GQ1b IgM antibodies. The present case might suggest a paraneoplastic asymmetrical and isolated hypoglossal nerve palsy associated with a new subset of anti-ganglioside antibodies.

DOI： 10.2169/internalmedicine.1269-18

Clinical Benefits of Antioxidative Supplement Twendee X for Mild Cognitive Impairment: A Multicenter, Randomized, Double-Blind, and Placebo-Controlled Prospective Interventional Study. 査読国際誌

Koh Tadokoro, Ryuta Morihara, Yasuyuki Ohta, Nozomi Hishikawa, Satoko Kawano, Ryo Sasaki, Namiko Matsumoto, Emi Nomura, Yumiko Nakano, Yoshiaki Takahashi, Mami Takemoto, Toru Yamashita, Setsuko Ueno, Yosuke Wakutani, Yoshiki Takao, Nobutoshi Morimoto, Yumiko Kutoku, Yoshihide Sunada, Katsushi Taomoto, Yasuhiro Manabe, Kentaro Deguchi, Yasuto Higashi, Haruhiko Inufusa, Fukka You, Toshikazu Yoshikawa, Markus Matuschka von Greiffenclau, Koji Abe

Journal of Alzheimer's disease : JAD 71 ( 3 ) 1063 - 1069 2019年

記述言語：英語掲載種別：研究論文（学術雑誌）

Oxidative stress is part of the entire pathological process that underlies the development of Alzheimer's disease (AD), including the mild cognitive impairment (MCI) stage. Twendee X (TwX) is a supplement containing a strong antioxidative mix of eight antioxidants, which has been shown to have a clinical and therapeutic benefit in AD model mice. Here, we conducted a multicenter, randomized, double-blind, and placebo-controlled prospective interventional study to evaluate the efficacy of TwX in mitigating MCI. The primary outcomes were differences in Mini-Mental State Examination (MMSE) and Hasegawa Dementia Scale-revised (HDS-R) scores between baseline and six months for placebo and TwX groups. Seventy-eight subjects with MCI were randomized into placebo (n = 37) and TwX (n = 41) groups. MMSE scores at six months differed significantly between the TwX and placebo groups (p = 0.018), and HDS-R scores for the TwX group exhibited a significant improvement at six months relative to baseline (p = 0.025). The TwX group did not show any change in affective or activities of daily living scores at six months. The present study indicates that strong antioxidative supplement TwX is clinical beneficial for cognitive function in subjects with MCI.

DOI： 10.3233/JAD-190644

Acute Anti-Inflammatory Markers ITIH4 and AHSG in Mice Brain of a Novel Alzheimer's Disease Model. 査読国際誌

Xiaowen Shi, Yasuyuki Ohta, Xia Liu, Jingwei Shang, Ryuta Morihara, Yumiko Nakano, Tian Feng, Yong Huang, Kota Sato, Mami Takemoto, Nozomi Hishikawa, Toru Yamashita, Koji Abe

Journal of Alzheimer's disease : JAD 68 ( 4 ) 1667 - 1675 2019年

記述言語：英語掲載種別：研究論文（学術雑誌）

Alzheimer's disease (AD) is the most common dementia and a progressive neurodegenerative disorder aggravated by chronic hypoperfusion (HP). Since numerous evidence suggests that inflammation is related with AD pathology, we investigated the expression change of two anti-inflammatory markers, inter-alpha-trypsin inhibitor heavy chain H4 (ITIH4) and alpha-2-HS-glycoprotein (AHSG), in a novel AD model (APP23) with HP at 12 month of age. As compared with wild type (WT, n = 10), immunohistochemical analysis showed a higher ITIH4 and a lower AHSG expressions in the cerebral cortex, hippocampus, and thalamus of the APP23 + HP group (n = 12) than the simple APP23 (n = 10) group (*p < 0.05 and **p < 0.01 versus WT; #p < 0.05 and # #p < 0.01 versus APP23). The present study provides an upregulation of anti-inflammatory ITIH4 and a downregulation of pro-inflammatory TNFα-dependent AHSG in a novel AD plus HP mice model.

DOI： 10.3233/JAD-181218

Clinical and Pathological Benefits of Edaravone for Alzheimer's Disease with Chronic Cerebral Hypoperfusion in a Novel Mouse Model. 査読国際誌

Tian Feng, Toru Yamashita, Jingwei Shang, Xiaowen Shi, Yumiko Nakano, Ryuta Morihara, Keiichiro Tsunoda, Emi Nomura, Ryo Sasaki, Koh Tadokoro, Namiko Matsumoto, Nozomi Hishikawa, Yasuyuki Ohta, Koji Abe

Journal of Alzheimer's disease : JAD 71 ( 1 ) 327 - 339 2019年

記述言語：英語掲載種別：研究論文（学術雑誌）

Alzheimer's disease (AD) and chronic cerebral hypoperfusion (CCH) often coexist in dementia patients in aging societies. The hallmarks of AD including amyloid-β (Aβ)/phosphorylated tau (pTau) and pathology-related events such as neural oxidative stress and neuroinflammation play critical roles in pathogenesis of AD with CCH. A large number of lessons from failures of drugs targeting a single target or pathway on this so complicated disease indicate that disease-modifying therapies targeting multiple key pathways hold potent potential in therapy of the disease. In the present study, we used a novel mouse model of AD with CCH to investigate a potential therapeutic effect of a free radical scavenger, Edaravone (EDA) on AD with CCH via examining motor and cognitive capacity, AD hallmarks, neural oxidative stress, and neuroinflammation. Compared with AD with CCH mice at 12 months of age, EDA significantly improved motor and cognitive deficits, attenuated neuronal loss, reduced Aβ/pTau accumulation, and alleviated neural oxidative stress and neuroinflammation. These findings suggest that EDA possesses clinical and pathological benefits for AD with CCH in the present mouse model and has a potential as a therapeutic agent for AD with CCH via targeting multiple key pathways of the disease pathogenesis.

DOI： 10.3233/JAD-190369

GPIHBP1 autoantibody syndrome during interferon β1a treatment

Jun Eguchi, Kazuya Miyashita, Isamu Fukamachi, Katsuyuki Nakajima, Masami Murakami, Yuko Kawahara, Toru Yamashita, Yasuyuki Ohta, Koji Abe, Atsuko Nakatsuka, Mai Mino, Satoru Takase, Hiroaki Okazaki, Robert A. Hegele, Michael Ploug, Xuchen Hu, Jun Wada, Stephen G. Young, Anne P. Beigneux

Journal of Clinical Lipidology 13 ( 1 ) 62 - 69 2019年

掲載種別：研究論文（学術雑誌）

© 2018 National Lipid Association Background: Autoantibodies against glycosylphosphatidylinositol-anchored high-density lipoprotein–binding protein 1 (GPIHBP1) cause chylomicronemia by blocking the ability of GPIHBP1 to bind lipoprotein lipase (LPL) and transport the enzyme to its site of action in the capillary lumen. Objective: A patient with multiple sclerosis developed chylomicronemia during interferon (IFN) β1a therapy. The chylomicronemia resolved when the IFN β1a therapy was discontinued. Here, we sought to determine whether the drug-induced chylomicronemia was caused by GPIHBP1 autoantibodies. Methods: We tested plasma samples collected during and after IFN β1a therapy for GPIHBP1 autoantibodies (by western blotting and with enzyme-linked immunosorbent assays). We also tested whether the patient's plasma blocked the binding of LPL to GPIHBP1 on GPIHBP1-expressing cells. Results: During IFN β1a therapy, the plasma contained GPIHBP1 autoantibodies, and those autoantibodies blocked GPIHBP1's ability to bind LPL. Thus, the chylomicronemia was because of the GPIHBP1 autoantibody syndrome. Consistent with that diagnosis, the plasma levels of GPIHBP1 and LPL were very low. After IFN β1a therapy was stopped, the plasma triglyceride levels returned to normal, and GPIHBP1 autoantibodies were undetectable. Conclusion: The appearance of GPIHBP1 autoantibodies during IFN β1a therapy caused chylomicronemia. The GPIHBP1 autoantibodies disappeared when the IFN β1a therapy was stopped, and the plasma triglyceride levels fell within the normal range.

DOI： 10.1016/j.jacl.2018.10.004

A unique case of hemi-tongue pseudohypertrophy, necrotizing myopathy, and erythema nodosum. 査読国際誌

Kota Sato, Yoshiaki Takahashi, Toru Yamashita, Mami Takemoto, Nozomi Hishikawa, Shang Jinwei, Yasuyuki Ohta, Koji Abe

Neurology international 10 ( 4 ) 7852 - 7852 2018年12月

記述言語：英語掲載種別：研究論文（学術雑誌）

A 46-year-old woman developed slowly progressive tongue weakness with a pseudohypertrophic change on the right side of her tongue. She subsequently developed weakness in her proximal lower extremities, skin erythema and a sustained increase of muscle enzymes at 11 M after the onset. A biopsy of the quadriceps muscle showed necrotizing myopathy and a skin biopsy showed erythema nodosum. The present case showed characteristic clinical manifestations that may represent a rare variant of sarcoidosis.

DOI： 10.4081/ni.2018.7852

Neurolymphomatosis in the Cauda Equina Diagnosed by an Open Biopsy. 査読

Ryo Sasaki, Yasuyuki Ohta, Yuto Yamada, Koh Tadokoro, Yoshiaki Takahashi, Kota Sato, Jingwei Shang, Mami Takemoto, Nozomi Hishikawa, Toru Yamashita, Takao Yasuhara, Isao Date, Shuntaro Ikegawa, Nobuharu Fujii, Koji Abe

Internal medicine (Tokyo, Japan) 57 ( 23 ) 3463 - 3465 2018年12月

記述言語：英語掲載種別：研究論文（学術雑誌）

Neurolymphomatosis is a rare form of extranodal malignant lymphoma defined as the infiltration of malignant lymphocytes into the central or peripheral nerve. We herein report a case of neurolymphomatosis in the cauda equina diagnosed by an open surgical biopsy. He presented with muscle weakness, atrophy, numbness and hypoesthesia in the bilateral lower extremities with the accumulation of 18fluoro-2-deoxyglucose (FDG) in the bilateral cauda equina. Cerebrospinal fluid cytology (three times) and flow cytometry (two times) and biopsies of the left sural nerve, bone marrow, paranasal sinus and left testis were all negative for malignancy, so finally we performed a surgical open biopsy of the cauda equina by laminectomy and diagnosed him with diffuse large B-cell lymphoma in the cauda equina. He was successfully treated with the disappearance of the FDG accumulation for a long time. The present case suggested that an early open biopsy of the cauda equina may be considered for cases of suspected neurolymphomatosis in the cauda equina for a good outcome.

DOI： 10.2169/internalmedicine.1049-18

Neuroprotective effects of SMTP-44D in mice stroke model in relation to neurovascular unit and trophic coupling. 査読国際誌

Xiaowen Shi, Yasuyuki Ohta, Jingwei Shang, Ryuta Morihara, Yumiko Nakano, Yusuke Fukui, Xia Liu, Tian Feng, Yong Huang, Kota Sato, Mami Takemoto, Nozomi Hishikawa, Toru Yamashita, Eriko Suzuki, Keiji Hasumi, Koji Abe

Journal of neuroscience research 96 ( 12 ) 1887 - 1899 2018年12月

記述言語：英語掲載種別：研究論文（学術雑誌）

Stachybotrys microspora triprenyl phenol (SMTP)-44D has both anti-oxidative and anti-inflammatory activities, but its efficacy has not been proved in relation to the pathological changes of neurovascular unit (NVU) and neurovascular trophic coupling (NVTC) in ischemic stroke. Here, the present study was designed to assess the efficacies of SMTP-44D, moreover, compared with the standard neuroprotective reagent edaravone in ischemic brains. ICR mice were subjected to transient middle cerebral artery occlusion (tMCAO) for 60 min, SMTP-44D (10 mg/kg) or edaravone (3 mg/kg) was intravenously administrated through subclavian vein just after the reperfusion, and these mice were examined at 1, 3, and 7 d after reperfusion. Compared with the vehicle group, SMTP-44D treatment revealed obvious ameliorations in clinical scores and infarct volume, meanwhile, markedly suppressed the accumulations of 4-HNE, 8-OHdG, nitrotyrosine, RAGE, TNF-α, Iba-1, and cleaved caspase-3 after tMCAO. In addition, SMTP-44D significantly prevented the dissociation of NVU and improved the intensity of NAGO/BDNF and the number of BDNF/TrkB and BDNF/NeuN double positive cells. These effects of SMTP-44D in reducing oxidative and inflammatory stresses were similar to or stronger than those of edaravone. The present study demonstrated that SMTP-44D showed strong anti-oxidative, anti-inflammatory, and anti-apoptotic effects, moreover, the drug also significantly improved the NVU damage and NVTC in the ischemic brain.

DOI： 10.1002/jnr.24326

Different clinicopathological features between Japanese siblings with facioscapulohumeral muscular dystrophy 2 with a novel nonsense SMCHD1 mutation (Arg552∗). 査読国際誌

Yasuyuki Ohta, Koh Tadokoro, Ryo Sasaki, Yoshiaki Takahashi, Kota Sato, Mami Takemoto, Nozomi Hishikawa, Jingwei Shang, Toru Yamashita, Yasushi Takehisa, Ichizo Nishino, Koji Abe

Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia 58 215 - 217 2018年12月

記述言語：英語掲載種別：研究論文（学術雑誌）

Facioscapulohumeral muscular dystrophy (FSHD) 2 is caused by a combination of heterozygous structural maintenance of chromosomes flexible hinge domain containing 1 (SMCHD1) mutation plus DNA hypomethylation on D4Z4. Here we report two Japanese FSHD2 siblings (brother and sister) with a new SMCHD1 nonsense mutation (a heterogeneous c. 1654C > T substitution, leading to a stop codon Arg552∗). They showed the typical phenotype of FSHD2 such as asymmetric muscle weakness and atrophy in bilateral facial, scapular and humeral muscles, but different clinicopathological features between them. The brother and asymptomatic mother showed normal D4Z4 methylation plus the same SMCHD1 mutation, but the sister showed the SMCHD1 mutation plus D4Z4 hypomethylation, suggesting an interesting correlation of the new SMCHD1 nonsense mutation and D4Z4 hypomethylation.

DOI： 10.1016/j.jocn.2018.10.021

Reduction of Ischemia Reperfusion-Related Brain Hemorrhage by Stachybotrys Microspora Triprenyl Phenol-7 in Mice With Antioxidant Effects. 査読国際誌

Yong Huang, Yasuyuki Ohta, Jingwei Shang, Xianghong Li, Xia Liu, Xiaowen Shi, Tian Feng, Toru Yamashita, Kota Sato, Mami Takemoto, Nozomi Hishikawa, Eriko Suzuki, Keiji Hasumi, Koji Abe

Journal of stroke and cerebrovascular diseases : the official journal of National Stroke Association 27 ( 12 ) 3521 - 3528 2018年12月

記述言語：英語掲載種別：研究論文（学術雑誌）

BACKGROUND: Stachybotrys microspora triprenyl phenol-7 (SMTP-7) has both thrombolytic and anti-inflammatory effects, but its neuroprotective effects on cerebral ischemia are still unclear. The present study assessed the antioxidative and neurovascular unit (NVU) protective effects of SMTP-7 using transient middle cerebral artery occlusion (tMCAO) mice. METHODS: After 60 minutes tMCAO, 0.9% NaCl, tissue-type plasminogen activator (tPA), SMTP-7 or tPA + SMTP-7 was intravenously administrated through subclavian vein just before the reperfusion, and these mice were examined at 24 hours after reperfusion. We histologically assessed the hemorrhage and expressive changes of antioxidative markers in brains. RESULTS: SMTP-7 treatment showed a similar antithrombotic effect to tPA, but significantly decreased the hemorrhage volumes and the number of 4-HNE, 3-NT and 8-OHdG positive cells, meanwhile, ameliorated the decrease of collagen IV in the ischemic brains. However, tPA + SMTP-7 treatment did not decrease hemorrhage volumes nor showed NVU protective effect. CONCLUSIONS: The present study suggested that SMTP-7 provided therapeutic benefits for ischemic stroke through antioxidative and NVU protective effects unlike tPA alone or tPA + SMTP-7.

DOI： 10.1016/j.jstrokecerebrovasdis.2018.08.018

Cervical compressive myelopathy caused by malfunction of a programmable cerebrospinal fluid shunt valve

Kota Sato, Toru Yamashita, Keichiro Tsunoda, Mami Takemoto, Nozomi Hishikawa, Jinwei Shang, Yasuyuki Ohta, Ken Kuwahara, Takao Yasuhara, Isao Date, Koji Abe

INTERDISCIPLINARY NEUROSURGERY-ADVANCED TECHNIQUES AND CASE MANAGEMENT 14 183 - 185 2018年12月

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

The primary treatment for hydrocephalus is ventricular shunt placement, and a programmable valve is widely used for ventriculoperitoneal (VP) shunt surgery to reduce over/under drainage of cerebrospinal fluid (CSF). Here, we report a rare case of a patient who developed successive VP shunt malfunction causing spastic muscle weakness in extremities associated cervical epidural venous distension and compressive myelopathy due to over-drainage of CSF through a defective VP shunt valve a decade after the initial shunt was placed. One should be aware and cognizant of this complication and carefully follow the symptoms and potentially utilize brain MRI with and without contrast to look at over drainage stigmata to avoid the development of neurological complications.

DOI： 10.1016/j.inat.2018.08.009

Antineuroinflammatory Effect of SMTP-7 in Ischemic Mice. 査読国際誌

Yong Huang, Yasuyuki Ohta, Jingwei Shang, Ryuta Morihara, Yumiko Nakano, Yusuke Fukui, Xia Liu, Xiaowen Shi, Tian Feng, Toru Yamashita, Kota Sato, Mami Takemoto, Nozomi Hishikawa, Eriko Suzuki, Keiji Hasumi, Koji Abe

Journal of stroke and cerebrovascular diseases : the official journal of National Stroke Association 27 ( 11 ) 3084 - 3094 2018年11月

記述言語：英語掲載種別：研究論文（学術雑誌）

BACKGROUND: Stachybotrys microspora triprenyl phenol-7 (SMTP-7) has both potentials of thrombolytic and neuroprotective effects, but its detailed neuroprotective mechanisms in ischemic stroke are still unclear. Here, we assessed the neuroprotective effects of SMTP-7 for anti-inflammatory and antiapoptosis mechanisms after 60 minutes of transient middle cerebral artery occlusion (tMCAO) in mice. METHODS: After 60minutes of tMCAO, 0.9% NaCl, tissue-type plasminogen activator (tPA), SMTP-7 or tPA+SMTP-7 was intravenously administrated through subclavian vein just before the reperfusion, and these mice were examined at 24hours after reperfusion. We histologically assessed the antineuroinflammatory effect of SMTP-7 on the expressive changes of inflammatory markers in ischemic mouse brains. RESULTS: Compared with the vehicle and tPA groups, SMTP-7 treatment significantly improved clinical scores and decreased the infarct volume and the numbers of TNF-α, nuclear factor-κB (NF-κB), nucleotide oligomerization domain-like receptor family pyrin domain containing 3 (NLRP3), and cleaved caspase-3-positive cells in the brain of mice at 24hours after tMCAO but not p62-positive cells. However, tPA+SMTP-7 treatment did not show such effects. CONCLUSIONS: The present study suggested that SMTP-7 provides a therapeutic benefit for ischemic stroke mice through anti-inflammatory and antiapoptotic effects but not antiautophagic effect.

DOI： 10.1016/j.jstrokecerebrovasdis.2018.06.039

A case of aspergillotic orbital apex syndrome diagnosed by an additional intraorbital biopsy after nasal endoscopy

Namiko Matsumoto, Kota Sato, Koh Tadokoro, Yoshiaki Takahashi, Taijun Yunoki, Mami Takemoto, Nozomi Hishikawa, Yasuyuki Ohta, Toru Yamashita, Kentaro Fujii, Tomotsugu Ichikawa, Isao Date, Koji Abe

NEUROLOGY AND CLINICAL NEUROSCIENCE 6 ( 6 ) 188 - 190 2018年11月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：WILEY

The prompt and accurate diagnosis of orbital apex syndrome (OAS) is very important because of its fatality. Here we report an old man with aspergillotic OAS diagnosed after two biopsies by nasal endoscopy and craniotomy. Only craniotomy leads to the appropriate diagnosis, suggesting an immediate need of additional biopsy for the accurate diagnosis and saving the patient.

DOI： 10.1111/ncn3.12226

Congenital myopathy with fiber-type disproportion accompanied by dilated cardiomyopathy in a patient with a novel p.G48A ACTA1 mutation. 査読国際誌

Koh Tadokoro, Yasuyuki Ohta, Ryo Sasaki, Yoshiaki Takahashi, Kota Sato, Jingwei Shang, Mami Takemoto, Nozomi Hishikawa, Toru Yamashita, Kazufumi Nakamura, Ichizo Nishino, Koji Abe

Journal of the neurological sciences 393 142 - 144 2018年10月

Chronic cerebral hypoperfusion accelerates Alzheimer's disease pathology with the change of mitochondrial fission and fusion proteins expression in a novel mouse model. 査読国際誌

Tian Feng, Toru Yamashita, Yun Zhai, Jingwei Shang, Yumiko Nakano, Ryuta Morihara, Yusuke Fukui, Nozomi Hishikawa, Yasuyuki Ohta, Koji Abe

Brain research 1696 63 - 70 2018年10月

記述言語：英語掲載種別：研究論文（学術雑誌）

Mitochondrial dynamically undergo massive fusion and fission events to continuously maintain their function in cells. Although an impaired balance of mitochondrial fission and fusion was reported in in-vitro and in-vivo Alzheimer's disease (AD) model, changes of mitochondrial fission and fusion proteins have not been reported in AD with chronic cerebral hypoperfusion (HP) as an etiological factor related to the development of elder AD. To clarify the impacts of HP on mitochondrial fission and fusion, related oxidative stress in the pathogenesis of AD, and protective effect of galantamine, the novel AD with HP mouse model (APP23 + HP) was applied in this project. Compared with APP23 mice, APP23 + HP mice greatly enhanced the number of Aβ oligomer-positive/phosphorylated tau (pTau) cells, the expression of mitochondrial fission proteins (Drp1 and Fis1), and decreased the expression of mitochondrial fusion proteins (Opa1 and Mfn1) in the cerebral cortex (CTX) and thalamus (TH) at 12 month (M) of age. Moreover, the expression of peroxidation products (4-HNE and 8-OHdG) showed a significant increase in CTX and TH of APP23 + HP mice at 12 M. However, above neuropathological characteristics were retrieved by galantamine (Gal) treatment, detected through immunohistochemical analyses. The present study demonstrates that cerebral HP shifted the balance in mitochondrial morphology from fusion to fission with increasing Aβ oligomer/pTau accumulations in APP23 mice, and such neuropathologic processes were strongly attenuated by Gal treatment.

DOI： 10.1016/j.brainres.2018.06.003

Protective effect of a novel sigma-1 receptor agonist is associated with reduced endoplasmic reticulum stress in stroke male mice. 査読国際誌

Ryuta Morihara, Toru Yamashita, Xia Liu, Yumiko Nakano, Yusuke Fukui, Kota Sato, Yasuyuki Ohta, Nozomi Hishikawa, Jingwei Shang, Koji Abe

Journal of neuroscience research 96 ( 10 ) 1707 - 1716 2018年10月

記述言語：英語掲載種別：研究論文（学術雑誌）

Sigma-1 receptor (Sig-1R) is expressed at endoplasmic reticulum (ER) membranes, where it regulates a variety of specific physiological functions. However, the profile and exact roles of ER stress-related molecules after Sig-1R agonist treatment in an in vivo stroke model are largely unknown. The aim of this study is to investigate the effect of a novel Sig-1R agonist, aniline derivative compound (Comp-AD), on the ER stress response following ischemic stroke. Male C57BL/6J mice received transient middle cerebral artery occlusion for 90 min, and were then treated with vehicle saline or Comp-AD at reperfusion. At 3 hr, 1 day, and 7 days after reperfusion, immunohis- tochemistry was performed for Sig-1R and ER stress-related proteins including phospho protein kinase RNA-like endoplasmic reticulum kinase (p-PERK), phospho inositol requiring enzyme 1α (p- IRE1α), and activating transcription factor 6 (ATF6). Neurobehavioral analysis showed improved functional recovery at 1 day and 7 days after reperfusion, and the infarct volume was significantly smaller at 7 days (p < .05), in the Comp-AD group compared with the vehicle group. Comp-AD treatment upregulated Sig-1R immunoreactivity at 3 hr and 1 day (p < .05), and reduced p-PERK and p-IRE1α expression at 1 day (p < .05, respectively), in the peri-ischemic region compared with the vehicle group. Treatment with the novel Sig-1R agonist Comp-AD was neuroprotective after transient middle cerebral artery occlusion, and was associated with upregulation of Sig-1R and a reduction of ER stress.

DOI： 10.1002/jnr.24270

Affective improvement of neurological disease patients and caregivers using an automated telephone call service. 査読国際誌

Yasuyuki Ohta, Toru Yamashita, Nozomi Hishikawa, Kota Sato, Noriko Hatanaka, Mami Takemoto, Shinji Doutare, Koji Abe

Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia 56 74 - 78 2018年10月

記述言語：英語掲載種別：研究論文（学術雑誌）

Neurological disease patients living alone or with a single caregiver need a support system to care for their psychological symptoms. We evaluated the clinical effects of a unique telephone call system that automatically called participants at their desired times once a week for 3 months. In total, 104 neurological disease patients and caregivers were evaluated by the geriatric depression scale, apathy scale and state and trait anxiety inventories (STAI) forms X-I for depression, apathy and state anxiety, respectively. High baseline STAI scores (40≥) significantly improved in the Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS), and spinocerebellar degeneration (SCD) + multiple system atrophy (MSA) patients (p = 0.001, p = 0.013 and p = 0.046, respectively) after patients/caregivers used the telephone call service. The baseline (pre) STAI score significantly correlated with the score change (post-pre) in PD, ALS, SCD + MSA, Alzheimer' s disease patients (ADp), and caregivers for ADp (p < 0.0001, p = 0.001, p = 0.011, p = 0.025 and p = 0.020, respectively). The geriatric depression scale and apathy scale did not significantly improve. The present study suggests that there is a positive effect of using an automated telephone call service for anxiety in neurological disease patients and caregivers, especially in ALS, SCD + MSA and PD patients with high STAI scores (40≥).

DOI： 10.1016/j.jocn.2018.07.006

Rare valiant vertical one-and-a-half syndrome without ipsilateral upward gaze palsy in a patient with thalamomesencephalic stroke 査読国際誌

Kota Sato, Yoshiaki Takahashi, Namiko Matsumoto, Taijun Yunoki, Mami Takemoto, Nozomi Hishikawa, Yasuyuki Ohta, Toru Yamashita, Koji Abe

NEUROLOGY AND CLINICAL NEUROSCIENCE 6 ( 5 ) 133 - 135 2018年9月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：WILEY

Bilateral upward and ipsilateral downward gaze palsy due to a unilateral thalamomesencephalic stroke is called vertical one-and-a-half syndrome (VOHS). Here, we report a valiant VOHS case who presented contralateral upward and ipsilateral downward gaze palsy due to a unilateral thalamomesencephalic stroke. The neuronal fiber connections associated with vertical gaze are not completely understood, so the present case provides an important proof to obtain a better understanding of vertical gaze mechanisms.

DOI： 10.1111/ncn3.12210

Vogt-Koyanagi-Harada case accompanied by polyneuropathy

Keiichiro Tsunoda, Yasuyuki Ohta, Koh Tadokoro, Ryo Sasaki, Yoshiaki Takahashi, Kota Sato, Emi Nomura, Mami Takemoto, Nozomi Hishikawa, Toru Yamashita, Ai Kajita, Koji Abe

NEUROLOGY AND CLINICAL NEUROSCIENCE 6 ( 5 ) 138 - 140 2018年9月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：WILEY

Vogt-Koyanagi-Harada disease (VKHD) is a systemic autoimmune disease that targets melanocyte-rich tissues such as eye, central nervous system, inner ear, and skin. Here, we report a case of VKHD accompanied by polyneuropathy. After VKHD was diagnosed, depending on the involvement of bilateral ocular, auditory, and central nervous systems, he expressed muscle weakness, pain, and numbness in bilateral lower extremities. Nerve conduction studies suggested sensorimotor polyneuropathy, while a skin, muscle, and nerve biopsy suggested vasculitis. Steroid therapy improved his symptoms. The present case might suggest a relationship between VKHD and polyneuropathy.

DOI： 10.1111/ncn3.12213

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