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Kazuki Tahara

Researcher at University of Illinois at Chicago

Publications -  6
Citations -  898

Kazuki Tahara is an academic researcher from University of Illinois at Chicago. The author has contributed to research in topics: Microglia & Alzheimer's disease. The author has an hindex of 6, co-authored 6 publications receiving 794 citations. Previous affiliations of Kazuki Tahara include University of Alabama at Birmingham.

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Role of toll-like receptor signalling in Aβ uptake and clearance

TL;DR: In this paper, the role of TLR4 in the amyloidogenesis in vivo, determined the amounts of cerebral Abeta in Alzheimer's disease mouse models with different genotypes of TLRs using three distinct methods.
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TLR4 mutation reduces microglial activation, increases Aβ deposits and exacerbates cognitive deficits in a mouse model of Alzheimer's disease

TL;DR: The results indicate that TLR4 is not involved in the initiation of Aβ deposition and that, as Aβ deposits start, microglia are activated viaTLR4 signaling to reduce A β deposits and preserve cognitive functions from Aβ-mediated neurotoxicity.
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Anti-Aβ single chain antibody delivery via adeno-associated virus for treatment of Alzheimer’s disease

TL;DR: A novel gene therapy modality where an adeno-associated virus (AAV) encoding anti-Aβ single-chain antibody (scFv) is injected into the corticohippocampal regions of AD mouse models may be a feasible solution for AD without eliciting inflammation.
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Amelioration of amyloid load by anti-Aβ single-chain antibody in Alzheimer mouse model

TL;DR: A human single-chain antibody (scFv) library for Abeta immunoreactivity is screened and a scFv that specifically reacts with oligomeric Abeta as well as amyloid plaques in the brain is isolated, which may be useful to treat AD patients without eliciting brain inflammation.

Role of toll-like receptor signalling in Ab uptake and clearance

TL;DR: The role of TLR4 in the amyloidogenesis in vivo was investigated in this article, where the amounts of cerebral Ab in Alzheimer's disease mouse models were determined using three distinct methods: immunocytochemistry, thioflavine-S staining and buffer-soluble and insoluble Ab by ELISA.