Researchers Database

sakiyama yoshio

    ComprehensiveMedicine1 Assistant Professor
Contact: sakiyamayjichi.ac.jp
Last Updated :2021/10/17

Researcher Information

Degree

  • Ph.D.(School of Medicine, University of Tokyo)

J-Global ID

Published Papers

  • Ayumi Hida, Takenari Yamashita, Yuji Hosono, Manami Inoue, Kenichi Kaida, Masato Kadoya, Yusuke Miwa, Nobuyuki Yajima, Reika Maezawa, Satoko Arai, Kazuhiro Kurasawa, Kazuhiro Ito, Hiroyuki Shimada, Tomoko Iwanami, Masahiro Sonoo, Yuki Hatanaka, Shigeo Murayama, Ayumi Uchibori, Atsuro Chiba, Hitoshi Aizawa, Takayuki Momoo, Yoshiharu Nakae, Yasuhisa Sakurai, Yasushi Shiio, Hideji Hashida, Toshihiro Yoshizawa, Yoshio Sakiyama, Aya Oda, Kiyoharu Inoue, Sousuke Takeuchi, Nobue K. Iwata, Hidetoshi Date, Naoki Masuda, Takashi Mikata, Yasufumi Motoyoshi, Yoshikazu Uesaka, Meiko Hashimoto Maeda, Ran Nakashima, Shoji Tsuji, Shin Kwak, Tsuneyo Mimori, Jun Shimizu
    NEUROLOGY 87 (3) 299 - 308 0028-3878 2016/07 [Refereed][Not invited]
     
    Objective: We aimed to analyze the clinical and histopathologic features of cancer-associated myositis (CAM) in relation to anti-transcriptional intermediary factor 1-gamma antibody (anti-TIF1 gamma-Ab), a marker of cancer association. Methods: We retrospectively studied 349 patients with idiopathic inflammatory myopathies (Ms), including 284 patients with pretreatment biopsy samples available. For the classification of Ms, the European Neuromuscular Center criteria were applied. Patients with CAM with (anti-TIF1-gamma-Ab[] CAM) and without anti-TIF1--y-Ab (anti-TIF1--y-Ab[] CAM) were compared with patients with IIM without cancers within and beyond 3 years of myositis diagnosis. Results: Cancer was detected in 75 patients, of whom 36 (48%) were positive for anti-TIF1--y-Ab. In anti-TIF1-gamma-Ab(+) patients with CAM, cancers were detected within 1 year of myositis diagnosis in 35 (97%) and before 1 year of myositis diagnosis in 1. All the anti-TIF1-gamma-Ab(+) patients with CAM satisfied the dermatomyositis (DM) criteria, including 2 possible DM sine dermatitis cases, and were characterized histologically by the presence of perifascicular atrophy, vacuolated fibers (VFs), and dense C5b-9 deposits on capillaries (dC5b-9). In contrast, 39 anti-TIF1-gamma-Ab() patients with CAM were classified into various subgroups, and characterized by a higher frequency of necrotizing autoimmune myopathy (NAM). Notably, all 7 patients with CAM classified into the NAM subgroup were anti-TIF1-gamma-Ab(+) and exhibited no dC5b-9 or VFs. Conclusions: CAM includes clinicohistopathologically heterogeneous disease entities. Among CAM entities, anti-TIF1-gamma-Ab(+) CAM has characteristically shown a close temporal association with cancer detection and the histopathologic findings of dC5b-9 and VFs, and CAM with NAM is a subset of anti-TIF1-gamma-Ab(+) CAM.
  • Shibata S, Sanayama H, Ono S, Sakiyama Y
    Journal of Japanese Congress on Neurological Emergencies (株)へるす出版事業部 28 (3) 30 - 34 1619-3067 2016/06 [Refereed][Not invited]
     
    症例は49歳男性で、複視と右眼瞼下垂を自覚した。構音障害、下肢脱力、続いて嚥下障害が出現した。筋力低下は進行して歩行困難となり、緊急入院となった。重症筋無力症の悪化と考えピリドスチグミン、プレドニゾロン内服を開始した。筋力は改善傾向を呈し歩行も可能となったが、第7病日未明に脱衣し病棟を徘徊、聴取困難な1独語や意思疎通困難となる異常言動が出現した。次第に呼吸状態が悪化したため気管挿管しICU管理とした。重症筋無力症クリーゼとして単純血漿交換療法3日間、ステロイドパルス療法、ガンマグロブリン大量静注療法(IVIg)による治療を開始した。また発熱と発汗、流涎が顕著であったことから、セロトニン症候群が疑われ、並行してプロポフォールによる鎮静とシプロヘプタジン投与を開始した。複数の医療機関から多種・多剤の抗精神病薬を処方され薬物依存状態にあったことが判明した。治療継続により症状改善が得られ、第49病日に自宅退院とした。
  • Michito Namekawa, Takeshi Yamashita, Yoshio Sakiyama
    Internal Medicine 55 (8) 1033 - 1033 1349-7235 2016/04 [Not refereed][Not invited]
  • Michito Namekawa, Takeshi Yamashita, Yoshio Sakiyama
    Internal Medicine 55 (8) 1033 - 1033 1349-7235 2016/04 [Not refereed][Not invited]
  • Michito Namekawa, Takeshi Yamashita, Yoshio Sakiyama
    Internal Medicine 55 (8) 1033 - 1033 1349-7235 2016/04 [Not refereed][Not invited]
  • Namekawa Michito, Yamashita Takeshi, Sakiyama Yoshio
    Internal Medicine 一般社団法人 日本内科学会 55 (8) 1033 - 1033 0918-2918 2016 [Not refereed][Not invited]
  • Namekawa Michito, Yamashita Takeshi, Sakiyama Yoshio
    Internal Medicine 一般社団法人 日本内科学会 55 (8) 1033 - 1033 0918-2918 2016 [Not refereed][Not invited]
  • Namekawa Michito, Yamashita Takeshi, Sakiyama Yoshio
    Internal Medicine 一般社団法人 日本内科学会 55 (8) 1033 - 1033 0918-2918 2016 [Not refereed][Not invited]
  • Namekawa Michito, Yamashita Takeshi, Sakiyama Yoshio
    Internal Medicine 一般社団法人 日本内科学会 55 (8) 1033 - 1033 0918-2918 2016 [Not refereed][Not invited]
  • Namekawa Michito, Yamashita Takeshi, Sakiyama Yoshio
    Internal Medicine 一般社団法人 日本内科学会 55 (8) 1033 - 1033 0918-2918 2016 [Not refereed][Not invited]
  • Namekawa Michito, Yamashita Takeshi, Sakiyama Yoshio
    Internal Medicine 一般社団法人 日本内科学会 55 (8) 1033 - 1033 0918-2918 2016 [Not refereed][Not invited]
  • Namekawa Michito, Yamashita Takeshi, Sakiyama Yoshio
    Internal Medicine 一般社団法人 日本内科学会 55 (8) 1033 - 1033 0918-2918 2016 [Not refereed][Not invited]
  • Namekawa Michito, Yamashita Takeshi, Sakiyama Yoshio
    Internal Medicine 一般社団法人 日本内科学会 55 (8) 1033 - 1033 0918-2918 2016 [Not refereed][Not invited]
  • Namekawa Michito, Yamashita Takeshi, Sakiyama Yoshio
    Internal Medicine 一般社団法人 日本内科学会 55 (8) 1033 - 1033 0918-2918 2016 [Not refereed][Not invited]
  • Namekawa Michito, Yamashita Takeshi, Sakiyama Yoshio
    Internal Medicine 一般社団法人 日本内科学会 55 (8) 1033 - 1033 0918-2918 2016 [Not refereed][Not invited]
  • Namekawa Michito, Yamashita Takeshi, Sakiyama Yoshio
    Internal Medicine 一般社団法人 日本内科学会 55 (8) 1033 - 1033 0918-2918 2016 [Not refereed][Not invited]
  • Namekawa Michito, Yamashita Takeshi, Sakiyama Yoshio
    Internal Medicine 一般社団法人 日本内科学会 55 (8) 1033 - 1033 0918-2918 2016 [Not refereed][Not invited]
  • Michito Namekawa, Takeshi Yamashita, Yoshio Sakiyama
    INTERNAL MEDICINE 55 (8) 1033 - 1033 0918-2918 2016 [Not refereed][Not invited]
  • Namekawa Michito, Yamashita Takeshi, Sakiyama Yoshio
    Internal Medicine 一般社団法人 日本内科学会 55 (8) 1033 - 1033 0918-2918 2016 [Not refereed][Not invited]
  • Namekawa Michito, Yamashita Takeshi, Sakiyama Yoshio
    Internal Medicine 一般社団法人 日本内科学会 55 (8) 1033 - 1033 0918-2918 2016 [Not refereed][Not invited]
  • Namekawa Michito, Yamashita Takeshi, Sakiyama Yoshio
    Internal Medicine 一般社団法人 日本内科学会 55 (8) 1033 - 1033 0918-2918 2016 [Not refereed][Not invited]
  • Namekawa Michito, Yamashita Takeshi, Sakiyama Yoshio
    Internal Medicine 一般社団法人 日本内科学会 55 (8) 1033 - 1033 0918-2918 2016 [Not refereed][Not invited]
  • Namekawa Michito, Yamashita Takeshi, Sakiyama Yoshio
    Internal Medicine 一般社団法人 日本内科学会 55 (8) 1033 - 1033 0918-2918 2016 [Not refereed][Not invited]
  • Namekawa Michito, Yamashita Takeshi, Sakiyama Yoshio
    Internal Medicine 一般社団法人 日本内科学会 55 (8) 1033 - 1033 0918-2918 2016 [Not refereed][Not invited]
  • Namekawa Michito, Yamashita Takeshi, Sakiyama Yoshio
    Internal Medicine 一般社団法人 日本内科学会 55 (8) 1033 - 1033 0918-2918 2016 [Not refereed][Not invited]
  • Namekawa Michito, Yamashita Takeshi, Sakiyama Yoshio
    Internal Medicine 一般社団法人 日本内科学会 55 (8) 1033 - 1033 0918-2918 2016 [Not refereed][Not invited]
  • Namekawa Michito, Yamashita Takeshi, Sakiyama Yoshio
    Internal Medicine 一般社団法人 日本内科学会 55 (8) 1033 - 1033 0918-2918 2016 [Not refereed][Not invited]
  • Namekawa Michito, Yamashita Takeshi, Sakiyama Yoshio
    Internal Medicine 一般社団法人 日本内科学会 55 (8) 1033 - 1033 0918-2918 2016 [Not refereed][Not invited]
  • Namekawa Michito, Yamashita Takeshi, Sakiyama Yoshio
    Internal Medicine 一般社団法人 日本内科学会 55 (8) 1033 - 1033 0918-2918 2016 [Not refereed][Not invited]
  • Namekawa M, Yamashita T, Sakiyama Y
    Internal medicine (Tokyo, Japan) 55 (8) 1033  0918-2918 2016 [Refereed][Not invited]
  • Namekawa Michito, Yamashita Takeshi, Sakiyama Yoshio
    Internal Medicine 一般社団法人 日本内科学会 55 (8) 1033 - 1033 0918-2918 2016 [Not refereed][Not invited]
  • Akane Nogami, Mineo Yamazaki, Yuko Saito, Hiroyuki Hatsuta, Yoshio Sakiyama, Masaki Takao, Kazumi Kimura, Shigeo Murayama
    JOURNAL OF NIPPON MEDICAL SCHOOL 82 (6) 266 - 273 1345-4676 2015/12 [Not refereed][Not invited]
     
    Diagnosing clinical progressive supranuclear palsy (PSP) is challenging. We hypothesize that there are more cases of pathological PSP than have been clinically identified, but its diagnosis is challenging because the initial lesions and progression of PSP have not yet been clarified. The purpose of our study was to clarify the incidence of PSP in consecutive autopsy cases and identify pathological characteristics of early PSP. We investigated 324 consecutive autopsy patients from a general geriatric hospital (age, mean SD=82.5 +/- 8.7 years). Paraffin sections of the midbrain were immunostained with anti 4-repeat tau antibodies (RD4). We selected cases showing RD4-positive neurofibrillary tangles and tufted astrocytes in the midbrain sections. Then, we used anti-phosphorylated tau antibody to immunostain sections from the basal ganglia, subthalamic nucleus, midbrain, pons, medulla, and cerebellum. Of the 324 patients, 35 had RD4-positive structures in the midbrain. From these 35 cases, we excluded those for which autopsies confirmed definite PSP (n=5) and cases of corticobasal degeneration (n=1), Alzheimer's disease (n=11), dementia of grain (n=10), and neurofibrillary tangles predominant forms of senile dementia (n=2), leaving 8 cases. We diagnosed these 8 cases as pure PSP-type tauopathy. Pure PSP-type tauopathy was detected in 2.5% of the consecutive autopsy cases, and this incidence was 1.6 times greater than that of neuropathologically definite PSP. This pure PSP-type tauopathy likely indicates preclinical stages of PSP. Furthermore, the novel neuropathological finding, which we term "pre clinical PSP," is unique and has not previously been reported. In order to elucidate the causes and pathological mechanisms of PSP, preclinical PSP should be investigated further.
  • Akane Nogami, Mineo Yamazaki, Yuko Saito, Hiroyuki Hatsuta, Yoshio Sakiyama, Masaki Takao, Kazumi Kimura, Shigeo Murayama
    JOURNAL OF NIPPON MEDICAL SCHOOL 82 (6) 266 - 273 1345-4676 2015/12 [Not refereed][Not invited]
     
    Diagnosing clinical progressive supranuclear palsy (PSP) is challenging. We hypothesize that there are more cases of pathological PSP than have been clinically identified, but its diagnosis is challenging because the initial lesions and progression of PSP have not yet been clarified. The purpose of our study was to clarify the incidence of PSP in consecutive autopsy cases and identify pathological characteristics of early PSP. We investigated 324 consecutive autopsy patients from a general geriatric hospital (age, mean SD=82.5 +/- 8.7 years). Paraffin sections of the midbrain were immunostained with anti 4-repeat tau antibodies (RD4). We selected cases showing RD4-positive neurofibrillary tangles and tufted astrocytes in the midbrain sections. Then, we used anti-phosphorylated tau antibody to immunostain sections from the basal ganglia, subthalamic nucleus, midbrain, pons, medulla, and cerebellum. Of the 324 patients, 35 had RD4-positive structures in the midbrain. From these 35 cases, we excluded those for which autopsies confirmed definite PSP (n=5) and cases of corticobasal degeneration (n=1), Alzheimer's disease (n=11), dementia of grain (n=10), and neurofibrillary tangles predominant forms of senile dementia (n=2), leaving 8 cases. We diagnosed these 8 cases as pure PSP-type tauopathy. Pure PSP-type tauopathy was detected in 2.5% of the consecutive autopsy cases, and this incidence was 1.6 times greater than that of neuropathologically definite PSP. This pure PSP-type tauopathy likely indicates preclinical stages of PSP. Furthermore, the novel neuropathological finding, which we term "pre clinical PSP," is unique and has not previously been reported. In order to elucidate the causes and pathological mechanisms of PSP, preclinical PSP should be investigated further.
  • Akane Nogami, Mineo Yamazaki, Yuko Saito, Hiroyuki Hatsuta, Yoshio Sakiyama, Masaki Takao, Kazumi Kimura, Shigeo Murayama
    JOURNAL OF NIPPON MEDICAL SCHOOL 82 (6) 266 - 273 1345-4676 2015/12 [Not refereed][Not invited]
     
    Diagnosing clinical progressive supranuclear palsy (PSP) is challenging. We hypothesize that there are more cases of pathological PSP than have been clinically identified, but its diagnosis is challenging because the initial lesions and progression of PSP have not yet been clarified. The purpose of our study was to clarify the incidence of PSP in consecutive autopsy cases and identify pathological characteristics of early PSP. We investigated 324 consecutive autopsy patients from a general geriatric hospital (age, mean SD=82.5 +/- 8.7 years). Paraffin sections of the midbrain were immunostained with anti 4-repeat tau antibodies (RD4). We selected cases showing RD4-positive neurofibrillary tangles and tufted astrocytes in the midbrain sections. Then, we used anti-phosphorylated tau antibody to immunostain sections from the basal ganglia, subthalamic nucleus, midbrain, pons, medulla, and cerebellum. Of the 324 patients, 35 had RD4-positive structures in the midbrain. From these 35 cases, we excluded those for which autopsies confirmed definite PSP (n=5) and cases of corticobasal degeneration (n=1), Alzheimer's disease (n=11), dementia of grain (n=10), and neurofibrillary tangles predominant forms of senile dementia (n=2), leaving 8 cases. We diagnosed these 8 cases as pure PSP-type tauopathy. Pure PSP-type tauopathy was detected in 2.5% of the consecutive autopsy cases, and this incidence was 1.6 times greater than that of neuropathologically definite PSP. This pure PSP-type tauopathy likely indicates preclinical stages of PSP. Furthermore, the novel neuropathological finding, which we term "pre clinical PSP," is unique and has not previously been reported. In order to elucidate the causes and pathological mechanisms of PSP, preclinical PSP should be investigated further.
  • Akane Nogami, Mineo Yamazaki, Yuko Saito, Hiroyuki Hatsuta, Yoshio Sakiyama, Masaki Takao, Kazumi Kimura, Shigeo Murayama
    JOURNAL OF NIPPON MEDICAL SCHOOL 82 (6) 266 - 273 1345-4676 2015/12 [Not refereed][Not invited]
     
    Diagnosing clinical progressive supranuclear palsy (PSP) is challenging. We hypothesize that there are more cases of pathological PSP than have been clinically identified, but its diagnosis is challenging because the initial lesions and progression of PSP have not yet been clarified. The purpose of our study was to clarify the incidence of PSP in consecutive autopsy cases and identify pathological characteristics of early PSP. We investigated 324 consecutive autopsy patients from a general geriatric hospital (age, mean SD=82.5 +/- 8.7 years). Paraffin sections of the midbrain were immunostained with anti 4-repeat tau antibodies (RD4). We selected cases showing RD4-positive neurofibrillary tangles and tufted astrocytes in the midbrain sections. Then, we used anti-phosphorylated tau antibody to immunostain sections from the basal ganglia, subthalamic nucleus, midbrain, pons, medulla, and cerebellum. Of the 324 patients, 35 had RD4-positive structures in the midbrain. From these 35 cases, we excluded those for which autopsies confirmed definite PSP (n=5) and cases of corticobasal degeneration (n=1), Alzheimer's disease (n=11), dementia of grain (n=10), and neurofibrillary tangles predominant forms of senile dementia (n=2), leaving 8 cases. We diagnosed these 8 cases as pure PSP-type tauopathy. Pure PSP-type tauopathy was detected in 2.5% of the consecutive autopsy cases, and this incidence was 1.6 times greater than that of neuropathologically definite PSP. This pure PSP-type tauopathy likely indicates preclinical stages of PSP. Furthermore, the novel neuropathological finding, which we term "pre clinical PSP," is unique and has not previously been reported. In order to elucidate the causes and pathological mechanisms of PSP, preclinical PSP should be investigated further.
  • Akane Nogami, Mineo Yamazaki, Yuko Saito, Hiroyuki Hatsuta, Yoshio Sakiyama, Masaki Takao, Kazumi Kimura, Shigeo Murayama
    JOURNAL OF NIPPON MEDICAL SCHOOL 82 (6) 266 - 273 1345-4676 2015/12 [Not refereed][Not invited]
     
    Diagnosing clinical progressive supranuclear palsy (PSP) is challenging. We hypothesize that there are more cases of pathological PSP than have been clinically identified, but its diagnosis is challenging because the initial lesions and progression of PSP have not yet been clarified. The purpose of our study was to clarify the incidence of PSP in consecutive autopsy cases and identify pathological characteristics of early PSP. We investigated 324 consecutive autopsy patients from a general geriatric hospital (age, mean SD=82.5 +/- 8.7 years). Paraffin sections of the midbrain were immunostained with anti 4-repeat tau antibodies (RD4). We selected cases showing RD4-positive neurofibrillary tangles and tufted astrocytes in the midbrain sections. Then, we used anti-phosphorylated tau antibody to immunostain sections from the basal ganglia, subthalamic nucleus, midbrain, pons, medulla, and cerebellum. Of the 324 patients, 35 had RD4-positive structures in the midbrain. From these 35 cases, we excluded those for which autopsies confirmed definite PSP (n=5) and cases of corticobasal degeneration (n=1), Alzheimer's disease (n=11), dementia of grain (n=10), and neurofibrillary tangles predominant forms of senile dementia (n=2), leaving 8 cases. We diagnosed these 8 cases as pure PSP-type tauopathy. Pure PSP-type tauopathy was detected in 2.5% of the consecutive autopsy cases, and this incidence was 1.6 times greater than that of neuropathologically definite PSP. This pure PSP-type tauopathy likely indicates preclinical stages of PSP. Furthermore, the novel neuropathological finding, which we term "pre clinical PSP," is unique and has not previously been reported. In order to elucidate the causes and pathological mechanisms of PSP, preclinical PSP should be investigated further.
  • Akane Nogami, Mineo Yamazaki, Yuko Saito, Hiroyuki Hatsuta, Yoshio Sakiyama, Masaki Takao, Kazumi Kimura, Shigeo Murayama
    JOURNAL OF NIPPON MEDICAL SCHOOL 82 (6) 266 - 273 1345-4676 2015/12 [Not refereed][Not invited]
     
    Diagnosing clinical progressive supranuclear palsy (PSP) is challenging. We hypothesize that there are more cases of pathological PSP than have been clinically identified, but its diagnosis is challenging because the initial lesions and progression of PSP have not yet been clarified. The purpose of our study was to clarify the incidence of PSP in consecutive autopsy cases and identify pathological characteristics of early PSP. We investigated 324 consecutive autopsy patients from a general geriatric hospital (age, mean SD=82.5 +/- 8.7 years). Paraffin sections of the midbrain were immunostained with anti 4-repeat tau antibodies (RD4). We selected cases showing RD4-positive neurofibrillary tangles and tufted astrocytes in the midbrain sections. Then, we used anti-phosphorylated tau antibody to immunostain sections from the basal ganglia, subthalamic nucleus, midbrain, pons, medulla, and cerebellum. Of the 324 patients, 35 had RD4-positive structures in the midbrain. From these 35 cases, we excluded those for which autopsies confirmed definite PSP (n=5) and cases of corticobasal degeneration (n=1), Alzheimer's disease (n=11), dementia of grain (n=10), and neurofibrillary tangles predominant forms of senile dementia (n=2), leaving 8 cases. We diagnosed these 8 cases as pure PSP-type tauopathy. Pure PSP-type tauopathy was detected in 2.5% of the consecutive autopsy cases, and this incidence was 1.6 times greater than that of neuropathologically definite PSP. This pure PSP-type tauopathy likely indicates preclinical stages of PSP. Furthermore, the novel neuropathological finding, which we term "pre clinical PSP," is unique and has not previously been reported. In order to elucidate the causes and pathological mechanisms of PSP, preclinical PSP should be investigated further.
  • Akane Nogami, Mineo Yamazaki, Yuko Saito, Hiroyuki Hatsuta, Yoshio Sakiyama, Masaki Takao, Kazumi Kimura, Shigeo Murayama
    JOURNAL OF NIPPON MEDICAL SCHOOL 82 (6) 266 - 273 1345-4676 2015/12 [Not refereed][Not invited]
     
    Diagnosing clinical progressive supranuclear palsy (PSP) is challenging. We hypothesize that there are more cases of pathological PSP than have been clinically identified, but its diagnosis is challenging because the initial lesions and progression of PSP have not yet been clarified. The purpose of our study was to clarify the incidence of PSP in consecutive autopsy cases and identify pathological characteristics of early PSP. We investigated 324 consecutive autopsy patients from a general geriatric hospital (age, mean SD=82.5 +/- 8.7 years). Paraffin sections of the midbrain were immunostained with anti 4-repeat tau antibodies (RD4). We selected cases showing RD4-positive neurofibrillary tangles and tufted astrocytes in the midbrain sections. Then, we used anti-phosphorylated tau antibody to immunostain sections from the basal ganglia, subthalamic nucleus, midbrain, pons, medulla, and cerebellum. Of the 324 patients, 35 had RD4-positive structures in the midbrain. From these 35 cases, we excluded those for which autopsies confirmed definite PSP (n=5) and cases of corticobasal degeneration (n=1), Alzheimer's disease (n=11), dementia of grain (n=10), and neurofibrillary tangles predominant forms of senile dementia (n=2), leaving 8 cases. We diagnosed these 8 cases as pure PSP-type tauopathy. Pure PSP-type tauopathy was detected in 2.5% of the consecutive autopsy cases, and this incidence was 1.6 times greater than that of neuropathologically definite PSP. This pure PSP-type tauopathy likely indicates preclinical stages of PSP. Furthermore, the novel neuropathological finding, which we term "pre clinical PSP," is unique and has not previously been reported. In order to elucidate the causes and pathological mechanisms of PSP, preclinical PSP should be investigated further.
  • Akane Nogami, Mineo Yamazaki, Yuko Saito, Hiroyuki Hatsuta, Yoshio Sakiyama, Masaki Takao, Kazumi Kimura, Shigeo Murayama
    JOURNAL OF NIPPON MEDICAL SCHOOL 82 (6) 266 - 273 1345-4676 2015/12 [Not refereed][Not invited]
     
    Diagnosing clinical progressive supranuclear palsy (PSP) is challenging. We hypothesize that there are more cases of pathological PSP than have been clinically identified, but its diagnosis is challenging because the initial lesions and progression of PSP have not yet been clarified. The purpose of our study was to clarify the incidence of PSP in consecutive autopsy cases and identify pathological characteristics of early PSP. We investigated 324 consecutive autopsy patients from a general geriatric hospital (age, mean SD=82.5 +/- 8.7 years). Paraffin sections of the midbrain were immunostained with anti 4-repeat tau antibodies (RD4). We selected cases showing RD4-positive neurofibrillary tangles and tufted astrocytes in the midbrain sections. Then, we used anti-phosphorylated tau antibody to immunostain sections from the basal ganglia, subthalamic nucleus, midbrain, pons, medulla, and cerebellum. Of the 324 patients, 35 had RD4-positive structures in the midbrain. From these 35 cases, we excluded those for which autopsies confirmed definite PSP (n=5) and cases of corticobasal degeneration (n=1), Alzheimer's disease (n=11), dementia of grain (n=10), and neurofibrillary tangles predominant forms of senile dementia (n=2), leaving 8 cases. We diagnosed these 8 cases as pure PSP-type tauopathy. Pure PSP-type tauopathy was detected in 2.5% of the consecutive autopsy cases, and this incidence was 1.6 times greater than that of neuropathologically definite PSP. This pure PSP-type tauopathy likely indicates preclinical stages of PSP. Furthermore, the novel neuropathological finding, which we term "pre clinical PSP," is unique and has not previously been reported. In order to elucidate the causes and pathological mechanisms of PSP, preclinical PSP should be investigated further.
  • Nogami Akane, Yamazaki Mineo, Saito Yuko, Hatsuta Hiroyuki, Sakiyama Yoshio, Takao Masaki, Kimura Kazumi, Murayama Shigeo
    Journal of Nippon Medical School 日本医科大学医学会 82 (6) 266 - 273 1345-4676 2015 [Not refereed][Not invited]
     
    Diagnosing clinical progressive supranuclear palsy (PSP) is challenging. We hypothesize that there are more cases of pathological PSP than have been clinically identified, but its diagnosis is challenging because the initial lesions and progression of PSP have not yet been clarified. The purpose of our study was to clarify the incidence of PSP in consecutive autopsy cases and identify pathological
  • Nogami Akane, Yamazaki Mineo, Saito Yuko, Hatsuta Hiroyuki, Sakiyama Yoshio, Takao Masaki, Kimura Kazumi, Murayama Shigeo
    Journal of Nippon Medical School 日本医科大学医学会 82 (6) 266 - 273 1345-4676 2015 [Not refereed][Not invited]
     
    Diagnosing clinical progressive supranuclear palsy (PSP) is challenging. We hypothesize that there are more cases of pathological PSP than have been clinically identified, but its diagnosis is challenging because the initial lesions and progression of PSP have not yet been clarified. The purpose of our study was to clarify the incidence of PSP in consecutive autopsy cases and identify pathological
  • Nogami Akane, Yamazaki Mineo, Saito Yuko, Hatsuta Hiroyuki, Sakiyama Yoshio, Takao Masaki, Kimura Kazumi, Murayama Shigeo
    Journal of Nippon Medical School 日本医科大学医学会 82 (6) 266 - 273 1345-4676 2015 [Not refereed][Not invited]
     
    Diagnosing clinical progressive supranuclear palsy (PSP) is challenging. We hypothesize that there are more cases of pathological PSP than have been clinically identified, but its diagnosis is challenging because the initial lesions and progression of PSP have not yet been clarified. The purpose of our study was to clarify the incidence of PSP in consecutive autopsy cases and identify pathological
  • Akane Nogami, Mineo Yamazaki, Yuko Saito, Hiroyuki Hatsuta, Yoshio Sakiyama, Masaki Takao, Kazumi Kimura, Shigeo Murayama
    Journal of Nippon Medical School = Nippon Ika Daigaku zasshi 82 (6) 266 - 73 1345-4676 2015 [Not refereed][Not invited]
     
    Diagnosing clinical progressive supranuclear palsy (PSP) is challenging. We hypothesize that there are more cases of pathological PSP than have been clinically identified, but its diagnosis is challenging because the initial lesions and progression of PSP have not yet been clarified. The purpose of our study was to clarify the incidence of PSP in consecutive autopsy cases and identify pathological characteristics of early PSP. We investigated 324 consecutive autopsy patients from a general geriatric hospital (age, mean±SD=82.5±8.7 years). Paraffin sections of the midbrain were immunostained with anti 4-repeat tau antibodies (RD4). We selected cases showing RD4-positive neurofibrillary tangles and tufted astrocytes in the midbrain sections. Then, we used anti-phosphorylated tau antibody to immunostain sections from the basal ganglia, subthalamic nucleus, midbrain, pons, medulla, and cerebellum. Of the 324 patients, 35 had RD4-positive structures in the midbrain. From these 35 cases, we excluded those for which autopsies confirmed definite PSP (n=5) and cases of corticobasal degeneration (n=1), Alzheimer's disease (n=11), dementia of grain (n=10), and neurofibrillary tangles predominant forms of senile dementia (n=2), leaving 8 cases. We diagnosed these 8 cases as pure PSP-type tauopathy. Pure PSP-type tauopathy was detected in 2.5% of the consecutive autopsy cases, and this incidence was 1.6 times greater than that of neuropathologically definite PSP. This pure PSP-type tauopathy likely indicates preclinical stages of PSP. Furthermore, the novel neuropathological finding, which we term "preclinical PSP," is unique and has not previously been reported. In order to elucidate the causes and pathological mechanisms of PSP, preclinical PSP should be investigated further.
  • Nogami Akane, Yamazaki Mineo, Saito Yuko, Hatsuta Hiroyuki, Sakiyama Yoshio, Takao Masaki, Kimura Kazumi, Murayama Shigeo
    Journal of Nippon Medical School 日本医科大学医学会 82 (6) 266 - 273 1345-4676 2015 [Not refereed][Not invited]
     
    Diagnosing clinical progressive supranuclear palsy (PSP) is challenging. We hypothesize that there are more cases of pathological PSP than have been clinically identified, but its diagnosis is challenging because the initial lesions and progression of PSP have not yet been clarified. The purpose of our study was to clarify the incidence of PSP in consecutive autopsy cases and identify pathological
  • Akane Nogami, Mineo Yamazaki, Yuko Saito, Hiroyuki Hatsuta, Yoshio Sakiyama, Masaki Takao, Kazumi Kimura, Shigeo Murayama
    Journal of Nippon Medical School = Nippon Ika Daigaku zasshi 82 (6) 266 - 73 1345-4676 2015 [Not refereed][Not invited]
     
    Diagnosing clinical progressive supranuclear palsy (PSP) is challenging. We hypothesize that there are more cases of pathological PSP than have been clinically identified, but its diagnosis is challenging because the initial lesions and progression of PSP have not yet been clarified. The purpose of our study was to clarify the incidence of PSP in consecutive autopsy cases and identify pathological characteristics of early PSP. We investigated 324 consecutive autopsy patients from a general geriatric hospital (age, mean±SD=82.5±8.7 years). Paraffin sections of the midbrain were immunostained with anti 4-repeat tau antibodies (RD4). We selected cases showing RD4-positive neurofibrillary tangles and tufted astrocytes in the midbrain sections. Then, we used anti-phosphorylated tau antibody to immunostain sections from the basal ganglia, subthalamic nucleus, midbrain, pons, medulla, and cerebellum. Of the 324 patients, 35 had RD4-positive structures in the midbrain. From these 35 cases, we excluded those for which autopsies confirmed definite PSP (n=5) and cases of corticobasal degeneration (n=1), Alzheimer's disease (n=11), dementia of grain (n=10), and neurofibrillary tangles predominant forms of senile dementia (n=2), leaving 8 cases. We diagnosed these 8 cases as pure PSP-type tauopathy. Pure PSP-type tauopathy was detected in 2.5% of the consecutive autopsy cases, and this incidence was 1.6 times greater than that of neuropathologically definite PSP. This pure PSP-type tauopathy likely indicates preclinical stages of PSP. Furthermore, the novel neuropathological finding, which we term "preclinical PSP," is unique and has not previously been reported. In order to elucidate the causes and pathological mechanisms of PSP, preclinical PSP should be investigated further.
  • Nogami Akane, Yamazaki Mineo, Saito Yuko, Hatsuta Hiroyuki, Sakiyama Yoshio, Takao Masaki, Kimura Kazumi, Murayama Shigeo
    Journal of Nippon Medical School 日本医科大学医学会 82 (6) 266 - 273 1345-4676 2015 [Not refereed][Not invited]
     
    Diagnosing clinical progressive supranuclear palsy (PSP) is challenging. We hypothesize that there are more cases of pathological PSP than have been clinically identified, but its diagnosis is challenging because the initial lesions and progression of PSP have not yet been clarified. The purpose of our study was to clarify the incidence of PSP in consecutive autopsy cases and identify pathological
  • Akane Nogami, Mineo Yamazaki, Yuko Saito, Hiroyuki Hatsuta, Yoshio Sakiyama, Masaki Takao, Kazumi Kimura, Shigeo Murayama
    Journal of Nippon Medical School = Nippon Ika Daigaku zasshi 82 (6) 266 - 73 1345-4676 2015 [Not refereed][Not invited]
     
    Diagnosing clinical progressive supranuclear palsy (PSP) is challenging. We hypothesize that there are more cases of pathological PSP than have been clinically identified, but its diagnosis is challenging because the initial lesions and progression of PSP have not yet been clarified. The purpose of our study was to clarify the incidence of PSP in consecutive autopsy cases and identify pathological characteristics of early PSP. We investigated 324 consecutive autopsy patients from a general geriatric hospital (age, mean±SD=82.5±8.7 years). Paraffin sections of the midbrain were immunostained with anti 4-repeat tau antibodies (RD4). We selected cases showing RD4-positive neurofibrillary tangles and tufted astrocytes in the midbrain sections. Then, we used anti-phosphorylated tau antibody to immunostain sections from the basal ganglia, subthalamic nucleus, midbrain, pons, medulla, and cerebellum. Of the 324 patients, 35 had RD4-positive structures in the midbrain. From these 35 cases, we excluded those for which autopsies confirmed definite PSP (n=5) and cases of corticobasal degeneration (n=1), Alzheimer's disease (n=11), dementia of grain (n=10), and neurofibrillary tangles predominant forms of senile dementia (n=2), leaving 8 cases. We diagnosed these 8 cases as pure PSP-type tauopathy. Pure PSP-type tauopathy was detected in 2.5% of the consecutive autopsy cases, and this incidence was 1.6 times greater than that of neuropathologically definite PSP. This pure PSP-type tauopathy likely indicates preclinical stages of PSP. Furthermore, the novel neuropathological finding, which we term "preclinical PSP," is unique and has not previously been reported. In order to elucidate the causes and pathological mechanisms of PSP, preclinical PSP should be investigated further.
  • Nogami Akane, Yamazaki Mineo, Saito Yuko, Hatsuta Hiroyuki, Sakiyama Yoshio, Takao Masaki, Kimura Kazumi, Murayama Shigeo
    Journal of Nippon Medical School 日本医科大学医学会 82 (6) 266 - 273 1345-4676 2015 [Not refereed][Not invited]
     
    Diagnosing clinical progressive supranuclear palsy (PSP) is challenging. We hypothesize that there are more cases of pathological PSP than have been clinically identified, but its diagnosis is challenging because the initial lesions and progression of PSP have not yet been clarified. The purpose of our study was to clarify the incidence of PSP in consecutive autopsy cases and identify pathological
  • Akane Nogami, Mineo Yamazaki, Yuko Saito, Hiroyuki Hatsuta, Yoshio Sakiyama, Masaki Takao, Kazumi Kimura, Shigeo Murayama
    Journal of Nippon Medical School = Nippon Ika Daigaku zasshi 82 (6) 266 - 73 1345-4676 2015 [Not refereed][Not invited]
     
    Diagnosing clinical progressive supranuclear palsy (PSP) is challenging. We hypothesize that there are more cases of pathological PSP than have been clinically identified, but its diagnosis is challenging because the initial lesions and progression of PSP have not yet been clarified. The purpose of our study was to clarify the incidence of PSP in consecutive autopsy cases and identify pathological characteristics of early PSP. We investigated 324 consecutive autopsy patients from a general geriatric hospital (age, mean±SD=82.5±8.7 years). Paraffin sections of the midbrain were immunostained with anti 4-repeat tau antibodies (RD4). We selected cases showing RD4-positive neurofibrillary tangles and tufted astrocytes in the midbrain sections. Then, we used anti-phosphorylated tau antibody to immunostain sections from the basal ganglia, subthalamic nucleus, midbrain, pons, medulla, and cerebellum. Of the 324 patients, 35 had RD4-positive structures in the midbrain. From these 35 cases, we excluded those for which autopsies confirmed definite PSP (n=5) and cases of corticobasal degeneration (n=1), Alzheimer's disease (n=11), dementia of grain (n=10), and neurofibrillary tangles predominant forms of senile dementia (n=2), leaving 8 cases. We diagnosed these 8 cases as pure PSP-type tauopathy. Pure PSP-type tauopathy was detected in 2.5% of the consecutive autopsy cases, and this incidence was 1.6 times greater than that of neuropathologically definite PSP. This pure PSP-type tauopathy likely indicates preclinical stages of PSP. Furthermore, the novel neuropathological finding, which we term "preclinical PSP," is unique and has not previously been reported. In order to elucidate the causes and pathological mechanisms of PSP, preclinical PSP should be investigated further.
  • Nogami Akane, Yamazaki Mineo, Saito Yuko, Hatsuta Hiroyuki, Sakiyama Yoshio, Takao Masaki, Kimura Kazumi, Murayama Shigeo
    Journal of Nippon Medical School 日本医科大学医学会 82 (6) 266 - 273 1345-4676 2015 [Not refereed][Not invited]
     
    Diagnosing clinical progressive supranuclear palsy (PSP) is challenging. We hypothesize that there are more cases of pathological PSP than have been clinically identified, but its diagnosis is challenging because the initial lesions and progression of PSP have not yet been clarified. The purpose of our study was to clarify the incidence of PSP in consecutive autopsy cases and identify pathological
  • Akane Nogami, Mineo Yamazaki, Yuko Saito, Hiroyuki Hatsuta, Yoshio Sakiyama, Masaki Takao, Kazumi Kimura, Shigeo Murayama
    Journal of Nippon Medical School = Nippon Ika Daigaku zasshi 82 (6) 266 - 73 1345-4676 2015 [Not refereed][Not invited]
     
    Diagnosing clinical progressive supranuclear palsy (PSP) is challenging. We hypothesize that there are more cases of pathological PSP than have been clinically identified, but its diagnosis is challenging because the initial lesions and progression of PSP have not yet been clarified. The purpose of our study was to clarify the incidence of PSP in consecutive autopsy cases and identify pathological characteristics of early PSP. We investigated 324 consecutive autopsy patients from a general geriatric hospital (age, mean±SD=82.5±8.7 years). Paraffin sections of the midbrain were immunostained with anti 4-repeat tau antibodies (RD4). We selected cases showing RD4-positive neurofibrillary tangles and tufted astrocytes in the midbrain sections. Then, we used anti-phosphorylated tau antibody to immunostain sections from the basal ganglia, subthalamic nucleus, midbrain, pons, medulla, and cerebellum. Of the 324 patients, 35 had RD4-positive structures in the midbrain. From these 35 cases, we excluded those for which autopsies confirmed definite PSP (n=5) and cases of corticobasal degeneration (n=1), Alzheimer's disease (n=11), dementia of grain (n=10), and neurofibrillary tangles predominant forms of senile dementia (n=2), leaving 8 cases. We diagnosed these 8 cases as pure PSP-type tauopathy. Pure PSP-type tauopathy was detected in 2.5% of the consecutive autopsy cases, and this incidence was 1.6 times greater than that of neuropathologically definite PSP. This pure PSP-type tauopathy likely indicates preclinical stages of PSP. Furthermore, the novel neuropathological finding, which we term "preclinical PSP," is unique and has not previously been reported. In order to elucidate the causes and pathological mechanisms of PSP, preclinical PSP should be investigated further.
  • Akane Nogami, Mineo Yamazaki, Yuko Saito, Hiroyuki Hatsuta, Yoshio Sakiyama, Masaki Takao, Kazumi Kimura, Shigeo Murayama
    Journal of Nippon Medical School = Nippon Ika Daigaku zasshi 82 (6) 266 - 73 1345-4676 2015 [Refereed][Not invited]
     
    Diagnosing clinical progressive supranuclear palsy (PSP) is challenging. We hypothesize that there are more cases of pathological PSP than have been clinically identified, but its diagnosis is challenging because the initial lesions and progression of PSP have not yet been clarified. The purpose of our study was to clarify the incidence of PSP in consecutive autopsy cases and identify pathological characteristics of early PSP. We investigated 324 consecutive autopsy patients from a general geriatric hospital (age, mean±SD=82.5±8.7 years). Paraffin sections of the midbrain were immunostained with anti 4-repeat tau antibodies (RD4). We selected cases showing RD4-positive neurofibrillary tangles and tufted astrocytes in the midbrain sections. Then, we used anti-phosphorylated tau antibody to immunostain sections from the basal ganglia, subthalamic nucleus, midbrain, pons, medulla, and cerebellum. Of the 324 patients, 35 had RD4-positive structures in the midbrain. From these 35 cases, we excluded those for which autopsies confirmed definite PSP (n=5) and cases of corticobasal degeneration (n=1), Alzheimer's disease (n=11), dementia of grain (n=10), and neurofibrillary tangles predominant forms of senile dementia (n=2), leaving 8 cases. We diagnosed these 8 cases as pure PSP-type tauopathy. Pure PSP-type tauopathy was detected in 2.5% of the consecutive autopsy cases, and this incidence was 1.6 times greater than that of neuropathologically definite PSP. This pure PSP-type tauopathy likely indicates preclinical stages of PSP. Furthermore, the novel neuropathological finding, which we term "preclinical PSP," is unique and has not previously been reported. In order to elucidate the causes and pathological mechanisms of PSP, preclinical PSP should be investigated further.
  • Nogami Akane, Yamazaki Mineo, Saito Yuko, Hatsuta Hiroyuki, Sakiyama Yoshio, Takao Masaki, Kimura Kazumi, Murayama Shigeo
    Journal of Nippon Medical School 日本医科大学医学会 82 (6) 266 - 273 1345-4676 2015 [Not refereed][Not invited]
     
    Diagnosing clinical progressive supranuclear palsy (PSP) is challenging. We hypothesize that there are more cases of pathological PSP than have been clinically identified, but its diagnosis is challenging because the initial lesions and progression of PSP have not yet been clarified. The purpose of our study was to clarify the incidence of PSP in consecutive autopsy cases and identify pathological
  • 最新臨床脳卒中学 下巻 -最新の診断と治療- XVI. 脳出血各論 特殊な脳出血 硬膜動静脈瘻
    崎山 快夫
    日本臨床 72 (増刊7) 408 - 412 2014 [Not refereed][Invited]
  • Abnormal copper metabolism in Niemann-Pick disease type C mimicking Wilson's disease
    Sakiyama Yoshio, Aya Narita, Shou Osawa, Eiji Nanba, Kousaku Ohno, Mieko Otsuka
    Neurology and Clinical Neuroscience 2 (6) 193 - 200 2014 [Refereed][Not invited]
  • Yoshio Sakiyama, Eri Watanabe, Mieko Otsuka, Taishi Hirahara, Shinichi Momomura, Yukiko Hayashi
    Clinical Neurology 54 (6) 489 - 494 0009-918X 2014 [Refereed][Not invited]
     
    The patient was a 53-year-old male. He showed steppage gait at the age of 11 and equinus foot at 13. He walked unaided with shoe-insoles to support his heels. Atrial fibrillation and cardiac hypertrophy were found in his 30s, and ventricular tachycardia (VT) was observed at the age of 48. Electrophysiological studies were performed, but VT was not sustained, symptomatic, or showed signs of infra-Hisian block, and a pacemaker was not indicated. At 53, he was introduced to a neurologist because of tetraplegia after the first episode of syncope. A spinal MR showed ossification of posterior longitudinal ligament (OPLL) and central cervical cord injury. Furthermore, he presented not only contracture in his shoulder, elbow, and ankles but also atrophy in his scapulohumeral and gastrocnemius muscles. In accordance with a diagnosis of Emery-Dreifuss muscular dystrophy (EDMD), provocative testing of VT was carried out, and a cardiac resynchronization therapy defibrillator (CRT-D) was implanted. Later, a mutation analysis of the LMNA gene disclosed a known missense mutation of p.Arg377His, and we diagnosed him as EDMD2 (laminopathy). Contractures could be the clue to diagnose EDMD and indicate the need for pacemakers and defibrillators in patients with cardiac conduction disorders.
  • Masaki Takao, Masahiro Aoyama, Kinya Ishikawa, Yoshio Sakiyama, Harumi Yomono, Yuko Saito, Hiroshi Kurisaki, Ban Mihara, Shigeo Murayama
    BMJ Case Reports 2011 1757-790X 2011 [Refereed][Not invited]
     
    Clinical phenotype of individuals with spinocerebellar ataxia 2 (SCA2) is characterised by cerebellar ataxia and cognitive impairment. Although L-dopa-responsive Parkinsonism is considered as a rare clinical presentation in SCA2, it has been brought to the attention of many neurologists in several studies. The authors report an autopsy case of SCA2 with Parkinsonism from a Japanese family using archival materials of our Brain Bank to describe unique neuropathologic findings. The individual clinically showed Parkinsonism as a predominant phenotype instead of cerebellar ataxia. Besides the classic SCA2 neuropathologic alterations, Lewy bodies and Lewy neurites were present in the brainstem nuclei. Genetic analysis revealed shorter abnormal expansion of CAG repeats (less than 39). In contrast, the authors could not find α-synuclein pathology in two SCA2 cases without Parkinsonism. The present case will provide a neuropathologic evidence of correlation between α-synucleinopathy and Parkinsonism of SCA2 as well as shed light on understanding the pathomechanism of Parkinsonism in SCA2. Copyright 2011 BMJ Publishing Group. All rights reserved.
  • Harumi S. Yomono, Hiroshi Kurisaki, Akira Hebisawa, Yoshio Sakiyama, Yuko Saito, Shigeo Murayama
    Clinical Neurology 50 (3) 156 - 162 0009-918X 2010 [Refereed][Not invited]
     
    This is the first autopsy case of SCA2 with parkinsonian phenotype. At the age of 46, the patient got symptoms of parkinsonism to which anti-parkinsonian drugs were effective. He had mosaic 38, 40 CAG repeat expansions on chromosome 12q23-24. being diagnosed as SCA2, and his mother and his son also had CAG expansions on the same locus. In addition to parkinsonism, he also exhibited autonomic disturbance, dementia, and mild cerebellar ataxia. Brain images revealed severe atrophy of pons and medulla oblongata, resembling MSA-C. HVA and 5-HIAA were reduced in the cerebrospinal fluid, and the heart-mediastinum (H/M) ratio in myocardial 123I-MIBG cintigram was decreased, which suggested Lewy body pathology. He died at the age of 75 and the autopsy revealed atrophy of the olivo-ponto-cerebellar (OPC) system and substantia nigra which was compatible to SCA2, although the OPC system atrophy was less severe than formerly reported SCA2 cases. The degrees of atrophy of the OPC system and substantia nigra might explain the predominancy of clinical symptoms. Anti-lC2 positive inclusions in the pontine nuclei, inferior olive nuclei, cerebellum and substantia nigra confirmed a polyglutamine disease. In addition, there were the anti-phosphorylated α-synuclein positive. Lewy body related pathological changes in the substantia nigra, the locus ceruleus, the dorsal motor nuclei of vagus, and the sympathetic nerve in the myocardium. Major genetic abnormalities related to Parkinson disease were not detected. As another case of SCA2 with Lewy body pathology was reported in Japan, the coexistence of SCA2 and Lewy body pathology may not be accidental. Since myocardial MIBG scincigram can predict Lewy body pathology, we should seek more clinical cases of SCA2 with Lewy body pathology.
  • Renpei Sengoku, Yuko Saito, Masako Ikemura, Hiroyuki Hatsuta, Yoshio Sakiyama, Kazutomi Kanemaru, Tomio Arai, Motoji Sawabe, Noriko Tanaka, Hideki Mochizuki, Kiyoharu Inoue, Shigeo Murayama
    JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY 67 (11) 1072 - 1083 0022-3069 2008/11 [Refereed][Not invited]
     
    We investigated the incidence and extent of Lewy body (LB)-related alpha-synucleinopathy (LBAS) in the olfactory bulb (OB) in 320 consecutive autopsy patients from a general geriatric hospital (mean aged 81.5 +/- 8.5 years). Paraffin sections were immunostained with anti-phosphorylated alpha-synuclein, tyrosine hydroxylase, phosphorylated tau, and amyloid beta antibodies. LBAS was found in 102 patients (31.9%) in the central nervous system, including the spinal cord; the OB was involved in 85 (26.6%). Among these 85 patients, 2 had LBAS only in the anterior olfactory nucleus, 14 in the peripheral OB only, and 69 in both areas. In 5 patients, Lewy bodies were found only in the OB by hematoxylin and eosin stain;, 3 of these patients had Alzheimer disease, and all had LBAS. Very few tyrosine hydroxylase-immunoreactive periglomerular cells exhibited LBAS. All 35 LBAS patients with pigmentation loss in the substantia nigra had LBAS in the OB. LBAS in the amygdala was more strongly correlated with LBAS in the anterior olfactory nucleus than with that in the OB periphery. LBAS did not correlate with systemic tauopathy or amyloid beta amyloidosis. These results indicate a high incidence of LBAS in the aging human OB; they also suggest that LBAS extends from the periphery to the anterior olfactory nucleus and results in clinical manifestations of LB disease.
  • Masako Ikemura, Yuko Saito, Renpei Sengoku, Yoshio Sakiyama, Hiroyuki Hatsuta, Kazutomi Kanemaru, Motoji Sawabe, Tomio Arai, Genta Ito, Takeshi Imatsubo, Masashi Fukayama, Shigeo Murayama
    JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY 67 (10) 945 - 953 0022-3069 2008/10 [Refereed][Not invited]
     
    Involvement of the peripheral autonomic nervous system is a core feature of Lewy body (LB) diseases, including Parkinson disease (PD), PD with dementia, and dementia with LBs. To investigate the potential use of skin biopsy for the diagnosis of LB diseases, we assessed anti-phosphorylated alpha-synuclein immunoreactivity in peripheral nerves in samples of skin from the abdominal wall and flexor surface of the upper arm in 279 prospectively studied consecutively autopsied patients whose data were registered at the Brain Bank for Aging Research between 2002 and 2005. Positive immunoreactivity was demonstrated in the unmyelinated fibers of the dermis in 20 of 85 patients with LB pathology in the CNS and the adrenal glands, the latter representing a substitute for peripheral autonomic nervous system sympathetic ganglia; no reactivity was seen in 194 patients without CNS LB pathology. In 142 retrospectively Studied patients autopsied from 1995 onward who had subclinical or clinical LB disease, the sensitivity of the positive skin immunoreactivity was 70% in PD and PD with dementia and 40% in dementia with LBs. Skin immunoreactivity was absent in cases of multiple-system atrophy, progressive nuclear palsy, and corticobasal degeneration. We demonstrate for the first time that the skin is involved and may be a highly specific and useful biopsy site for the pathological diagnosis of LB diseases.
  • Murayama S, Saito Y, Hatsuta H, Sakiyama Y
    Nihon rinsho. Japanese journal of clinical medicine 8 65 1401 - 1406 0047-1852 2007/08 [Refereed][Not invited]

MISC

Awards & Honors

  • 2008/04 American Association of Neuropathologists Moore Award for Best Paper on Clinico-Pathological Correlation Presented at the Annual Meeting
     Incidence and Extent of Lewy Body-Related α-synucleinopathy in Human Aging Olfactory Bulb 
    受賞者: R. Sengoku;Y. Saito;M. Ikemura;H. Hatsuta;Y. Sakiyama;M. Sawabe;K. Inoue;H. Mochizuki;S. Muryama


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