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Kenji Ikeda

Researcher at Institute of Medical Science

Publications -  159
Citations -  8760

Kenji Ikeda is an academic researcher from Institute of Medical Science. The author has contributed to research in topics: Corticobasal degeneration & Senile plaques. The author has an hindex of 43, co-authored 157 publications receiving 8059 citations. Previous affiliations of Kenji Ikeda include Kagawa University.

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TDP-43 is a component of ubiquitin-positive tau-negative inclusions in frontotemporal lobar degeneration and amyotrophic lateral sclerosis

TL;DR: The common occurrence of intracellular accumulations of TDP-43 supports the hypothesis that these disorders represent a clinicopathological entity of a single disease, and suggests that they can be newly classified as a proteinopathy of T DP-43.
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Occurrence of T cells in the brain of Alzheimer's disease and other neurological diseases.

TL;DR: The phenotype of T cells in the AD brain indicates that they are activated but are not fully differentiated, and local inflammatory conditions might cause accumulation and activation of T cell in theAD brain.
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Cell mediators of inflammation in the Alzheimer disease brain.

TL;DR: In vivo and in vitro studies showed the effective uptake of A beta by microglia, and evidence also indicates that these cells eliminate A beta from the brain.
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Distinct isoforms of tau aggregated in neurons and glial cells in brains of patients with Pick's disease, corticobasal degeneration and progressive supranuclear palsy.

TL;DR: Investigation of isoform composition of aggregated tau protein in brains with Pick's disease, corticobasal degeneration and progressive supranuclear palsy by immunoblot analysis of sarkosyl-insoluble fractions of brain homogenates suggests tau isoforms involved in the pathological processes differ between CBD/PSP and PiD, and are thus disease specific.
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Thrombin accumulation in brains of patients with Alzheimer's disease.

TL;DR: Thrombin was detected immunohistochemically in brain tissue of Alzheimer's disease patients and age-matched controls, suggesting that thrombin formation from prothrombin probably takes place in AD brain.