Rachel Butler

TL;DR: It is shown that transplanted rod precursors can reform an anatomically distinct and appropriately polarized outer nuclear layer of photoreceptor cells, and visual function was restored in animals with zero rod function at baseline, suggesting that a cell therapy approach may reconstitute a light-sensitive cell layer de novo and repair a structurally damaged visual circuit.

TL;DR: The potential therapeutic pathways through which histone deacetylase inhibitors might act to correct the aberrant transcription observed in Huntington's disease and other polyglutamine repeat diseases are discussed.

TL;DR: When strain background and CAG repeat length are controlled for, the knock-in and fragment models develop comparable phenotypes, which supports the continued use of the more high-throughput fragment models to identify mechanisms of pathogenesis and for preclinical screening.

TL;DR: Reduction of HDAC4 levels in mouse models of Huntington's disease delays cytoplasmic aggregation in the brain and improves the molecular pathology of HD, providing a potential new therapeutic target.

TL;DR: A genetic cross to determine whether genetic reduction of Hdac7 would alleviate phenotypes in the R6/2 mice found no improvement in a number of physiological or behavioral phenotypes, suggesting that the beneficial effects ofHDAC inhibitors are not predominantly mediated through the inhibition of HDAC7.