Hitoshi Takahashi

TL;DR: It is found that CBP was depleted from its normal nuclear location and was present in polyglutamine aggregates in HD cell culture models, HD transgenic mice, and human HD postmortem brain, suggesting polyglUTamine-mediated interference with CBP-regulated gene transcription may constitute a genetic gain of function, underlying the pathogenesis of polyglutsamine disorders.

TL;DR: It is proposed that the wide variety of clinical manifestations of DRPLA can now be explained by the variable unstable expansion of the CAG repeat.

TL;DR: A novel strategy, the direct identification of repeat expansion and cloning technique (DIRECT), which allows selective detection of expanded GAG repeats and cloning of the genes involved and will dramatically accelerate the search for causative genes of neuropsychiatric diseases caused by trinucleotide repeat expansions.

TL;DR: Findings indicate that alpha-synuclein is also a major component of GCIs and NCIs in MSA and strongly suggest thatalpha- Synuclein aggregation is a common process in certain neurodegenerative diseases, including PD and MSA.

TL;DR: It is demonstrated that the immunoreactivities of AQP4 and GFAP were consistently lost from the early stage of the lesions in NMO, notably in the perivascular regions with complement and immunoglobulin deposition.