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Hiroaki Adachi

Researcher at University of East Anglia

Publications -  193
Citations -  13441

Hiroaki Adachi is an academic researcher from University of East Anglia. The author has contributed to research in topics: Spinal and bulbar muscular atrophy & Motor neuron. The author has an hindex of 47, co-authored 184 publications receiving 11914 citations. Previous affiliations of Hiroaki Adachi include Norwich Research Park & University of Occupational and Environmental Health Japan.

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Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

Daniel J. Klionsky, +2522 more
- 21 Jan 2016 - 
TL;DR: In this paper, the authors present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macro-autophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
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Testosterone reduction prevents phenotypic expression in a transgenic mouse model of spinal and bulbar muscular atrophy.

TL;DR: The results suggest the therapeutic potential of hormonal intervention for SBMA, and nuclear translocation of the mutant AR by testosterone contributed to the phenotypic difference with gender and the effects of hormonal interventions.
Journal ArticleDOI

17-AAG, an Hsp90 inhibitor, ameliorates polyglutamine-mediated motor neuron degeneration.

TL;DR: Administration of 17-AAG markedly ameliorated motor impairments in the SBMA transgenic mouse model without detectable toxicity and would provide a new therapeutic approach to SBMA and probably to other related neurodegenerative diseases.
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Leuprorelin rescues polyglutamine-dependent phenotypes in a transgenic mouse model of spinal and bulbar muscular atrophy

TL;DR: Leuprorelin, a lutenizing hormone–releasing hormone (LHRH) agonist that reduces testosterone release from the testis, rescued motor dysfunction and nuclear accumulation of mutant androgen receptors in male transgenic mice and seems to be a promising candidate for the treatment of SBMA.