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Hidetoshi Date

Researcher at University of Tokyo

Publications -  14
Citations -  1753

Hidetoshi Date is an academic researcher from University of Tokyo. The author has contributed to research in topics: Trinucleotide repeat expansion & Aprataxin. The author has an hindex of 13, co-authored 14 publications receiving 1430 citations.

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CpG Demethylation Enhances Alpha-Synuclein Expression and Affects the Pathogenesis of Parkinson's Disease

TL;DR: The findings suggest that a novel epigenetic regulatory mechanism controlling SNCA expression influences PD pathogenesis, and this CpG region may function as an intronic regulatory element for S NCA gene.
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Mutations in COQ2 in familial and sporadic multiple-system atrophy the multiple-system atrophy research collaboration

Jun Mitsui, +74 more
TL;DR: Functionally impaired variants of COQ2 were associated with an increased risk of multiple-system atrophy in multiplex families and patients with sporadic disease, providing evidence of a role of impaired COQ1 activities in the pathogenesis of this disease.
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Noncoding CGG repeat expansions in neuronal intranuclear inclusion disease, oculopharyngodistal myopathy and an overlapping disease.

TL;DR: Whole-genome sequencing identifies noncoding CGG repeat expansions in neuronal intranuclear inclusion disease, oculopharyngodistal myopathy and Oculopharyngealmyopathy with leukoencephalopathy, three disorders with overlapping clinical features and neuroimaging findings.
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Expansions of intronic TTTCA and TTTTA repeats in benign adult familial myoclonic epilepsy.

TL;DR: It is shown that abnormal expansions of TTTCA and TTTTA repeats in intron 4 of SAMD12 cause benign adult familial myoclonic epilepsy (BAFME), and RNA toxicity as the mechanism underlying disease pathogenesis is identified.
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IFNβ-1b may severely exacerbate Japanese optic-spinal MS in neuromyelitis optica spectrum

TL;DR: It is suggested that IFNβ-1b may trigger severe exacerbation in patients with the NMO spectrum and cases in N MO spectrum should be carefully excluded in INFβ- 1b therapy.