JaLCDOI 10.18926/AMO/56066
フルテキストURL 72_3_211.pdf
著者 Ikeda, Chikako| Yokota, Osamu| Miki, Tomoko| Takenoshita, Shintaro| Ishizu, Hideki| Terada, Seishi| Yamada, Norihito|
抄録 Neurodegenerative diseases in which tau accumulation plays a cardinal role in the pathogenic process are called tauopathies, and when tau isoforms having four repeats of the microtubule binding sites, four-repeat tau, are selectively accumulated as pathological hallmarks, the term four-repeat tauopathy is used. The major four-repeat tauopathies are progressive supranuclear palsy (PSP), corticobasal degeneration (CBD), and argyrophilic grain disease (AGD). Historically, neuronal cytopathologies, e.g., neurofibrillary tangles and ballooned neurons, were emphasized as characteristic lesions in PSP and CBD. Now, however, astrocytic tau pathologies, i.e., tufted astrocytes (TAs) and astrocytic plaques (APs), are considered to be highly disease-specific lesions. Although granular/fuzzy astrocytes (GFAs) frequently develop in the limbic system in AGD cases, the specificity is not conclusive yet. Some AGD cases have a few TAs, and to a lesser frequency, a few APs in the frontal cortex and subcortical nuclei. The number of astrocytic tau pathologies including TAs and GFAs increases with the progression of AGD. In this paper, histopathological features of astrocytic tau pathologies in PSP, CBD, and AGD are first reviewed. Then, recent findings regarding the coexistence of these tauopathies are summarized from a viewpoint of astrocytic tau pathologies. Further biochemical and pathological studies focusing tau-positive astrocytic lesions may be useful to increase understanding of the pathological process in four-repeat tauopathies and to develop novel therapeutic strategies for patients with these diseases.
キーワード astrocytic plaque four-repeat tau globular glial inclusion granular fuzzy astrocyte tufted astrocyte
Amo Type Review
発行日 2018-06
出版物タイトル Acta Medica Okayama
72巻
3号
出版者 Okayama University Medical School
開始ページ 211
終了ページ 221
ISSN 0386-300X
NCID AA00508441
資料タイプ 学術雑誌論文
言語 English
著作権者 CopyrightⒸ 2018 by Okayama University Medical School
論文のバージョン publisher
査読 有り
PubMed ID 29925998
JaLCDOI 10.18926/AMO/32652
フルテキストURL fulltext.pdf
著者 Inoue, Koutaro| Morimoto, Kiyoshi| Sato, Keiko| Yamada, Norihito| Otsuki, Saburo|
抄録 <p>A new model of status epilepticus (SE), which was induced by intermittent electrical stimulation (20 Hz for 20 sec every min for 180 min) of the deep prepyriform cortex, has been developed in the conscious rat. SE was induced in 9 of 16 rats in the drug-free group. The number of stimulation trains required to induce SE in this status subgroup was 125.6 +/- 12.7 (mean +/- SEM) and the mean duration of self-sustained seizure activity (SSSA) occurring after cessation of the stimulation session was 295.4 +/- 111.4 min. Some animals showed secondary generalized seizures. Significant cell loss was observed in the hippocampal CA3 pyramidal cell layer ipsilateral to the stimulation site and bilateral CA1 areas in the status subgroup compared with the group subjected to sham operation. In addition, there was a significant negative correlation between the duration of SSSA subsequent to the stimulation session and the total number of intact pyramidal neurons observed in the bilateral CA1 and ipsilateral CA3 subfields of the status subgroup. There were significant differences between the status and non-status subgroups with respect to the number of afterdischarges (ADs) and the total AD duration during the stimulation session. Pretreatment with phenobarbital (30 mg/kg) prevented the development of SE and hippocampal cell loss completely. Pretreatment with MK-801, a non-competitive N-methyl-D-aspartate (NMDA) receptor antagonist (0.25 or 1 mg/kg), also prevented hippocampal cell loss, although it did not block SE generation completely, which suggests dissociation of the mechanisms underlying the development of SE and hippocampal damage. These results indicate that prolonged SSSA actually causes hippocampal damage and it is critically dependent upon NMDA receptor participation.</p>
キーワード status epilepticus deep prepyriform cortex electrical stimulation hippcampus N-methl-D-aspartate(NMDA) ??-aminobutyric acid(GABA)
Amo Type Article
発行日 1992-04
出版物タイトル Acta Medica Okayama
46巻
2号
出版者 Okayama University Medical School
開始ページ 129
終了ページ 139
ISSN 0386-300X
NCID AA00508441
資料タイプ 学術雑誌論文
言語 English
論文のバージョン publisher
査読 有り
PubMed ID 1533485
Web of Sience KeyUT A1992HR48400010
JaLCDOI 10.18926/AMO/30752
フルテキストURL fulltext.pdf
著者 Yamamoto, Shin| Kitamura, Yoshihiro| Yamada, Norihito| Nakashima, Yoshihiko| Kuroda, Shigetoshi|
抄録 <p>Previous EEG studies have shown that transcendental meditation (TM) increases frontal and central alpha activity. The present study was aimed at identifying the source of this alpha activity using magnetoencephalography (MEG) and electroencephalography (EEG) simultaneously on eight TM practitioners before, during, and after TM. The magnetic field potentials corresponding to TM-induced alpha activities on EEG recordings were extracted, and we attempted to localize the dipole sources using the multiple signal classification (MUSIC) algorithm, equivalent current dipole source analysis, and the multiple spatio-temporal dipole model. Since the dipoles were mapped to both the medial prefrontal cortex (mPFC) and anterior cingulate cortex (ACC), it is suggested that the mPFC and ACC play an important role in brain activity induced by TM.</p>
キーワード transcendental meditation magnetoencephalography(MEG) source analysis medial prefrontal cortex anterior cingulate cortex
Amo Type Article
発行日 2006-02
出版物タイトル Acta Medica Okayama
60巻
1号
出版者 Okayama University Medical School
開始ページ 51
終了ページ 58
ISSN 0386-300X
NCID AA00508441
資料タイプ 学術雑誌論文
言語 English
論文のバージョン publisher
査読 有り
PubMed ID 16508689
Web of Sience KeyUT 000235538900006