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Toshihiko Suenaga

Researcher at Tenri Hospital

Publications -  79
Citations -  2206

Toshihiko Suenaga is an academic researcher from Tenri Hospital. The author has contributed to research in topics: Neuromyelitis optica & Magnetic resonance imaging. The author has an hindex of 22, co-authored 74 publications receiving 1919 citations. Previous affiliations of Toshihiko Suenaga include National Archives and Records Administration & Kyoto University.

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Effects of Extracranial–Intracranial Bypass for Patients With Hemorrhagic Moyamoya Disease: Results of the Japan Adult Moyamoya Trial

TL;DR: Although statistically marginal, Kaplan–Meier analysis revealed the significant difference between surgical and nonsurgical group, suggesting the preventive effect of direct bypass against rebleeding.
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Alterations of the blood-brain barrier and glial cells in white-matter lesions in cerebrovascular and Alzheimer's disease patients

TL;DR: The underlying cause of white-matter lesions, which are frequent findings in cerebrovascular disease (CVD) and Alzheimer's disease (AD), remains uncertain in this article.
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Alterations in glia and axons in the brains of Binswanger's disease patients.

TL;DR: The results indicate that an inflammatory reaction and compromised axonal transport, mediated by chronic ischemia, may play an important role in the pathophysiology of Binswanger's disease.
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Regressive changes of astroglia in white matter lesions in cerebrovascular disease and Alzheimer’s disease patients

TL;DR: In this paper, the authors used light and electron microscopic immunohistochemistry for glial fibrillary acidic protein (GFAP) as a marker, and found that clasmatodendritic astroglia had condensed chromatin, lysosomes and large membrane-bound osmiophilic cytoplasmic inclusions.
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Blood-brain barrier dysfunction in Binswanger's disease; an immunohistochemical study.

TL;DR: The results indicate that WM lesions in Binswanger’s disease are accompanied by blood-brain barrier dysfunction, although it remains uncertain whether BBB dysfunction is secondary to either chronic cerebral ischemia or arterial hypertension.