scispace - formally typeset
H

Hodaka Yamakado

Researcher at Kyoto University

Publications -  54
Citations -  1147

Hodaka Yamakado is an academic researcher from Kyoto University. The author has contributed to research in topics: Parkinson's disease & Substantia nigra. The author has an hindex of 16, co-authored 44 publications receiving 764 citations. Previous affiliations of Hodaka Yamakado include University of California, San Diego.

Papers
More filters
Journal ArticleDOI

Inoculation of α-synuclein preformed fibrils into the mouse gastrointestinal tract induces Lewy body-like aggregates in the brainstem via the vagus nerve

TL;DR: Results indicate that α-Syn PFF inoculation into the mouse gastrointestinal tract can induce α- synuclein pathology resembling that of very early PD, but other factors are apparently required if further progression of PD pathology is to be replicated in this animal model.
Journal ArticleDOI

Immunotherapy targeting toll-like receptor 2 alleviates neurodegeneration in models of synucleinopathy by modulating α-synuclein transmission and neuroinflammation.

TL;DR: This study proposes TLR2 immunotherapy as a novel therapeutic strategy for synucleinopathies of the aging population and demonstrated that administration of anti-TLR2 alleviated α-synuclein accumulation in neuronal and astroglial cells, neuroinflammation, neurodegeneration, and behavioral deficits in an α- Synuclein tg mouse model of PD/DLB.
Journal ArticleDOI

Cellular internalization of alpha-synuclein aggregates by cell surface heparan sulfate depends on aggregate conformation and cell type.

TL;DR: It is shown, using a pH-sensitive probe, that internalization of α-synuclein amyloid fibrils in neuroblastoma cells is dependent on heparan sulfate, whereasInternalization of smaller non-amyloid oligomers is not, and overall sulfation of the heparans sulfate chains is more important than sulfation at particular sites along the chains.
Journal ArticleDOI

Viable neuronopathic Gaucher disease model in Medaka (Oryzias latipes) displays axonal accumulation of alpha-synuclein.

TL;DR: GBA-/- medaka is revealed as a novel neuronopathic GD model, the pahological mechanisms of α-syn accumulation caused by GCase deficiency, and the minimal contribution ofα-syn to the pathogenesis of neuronopathicGD are revealed.