Ellen Sapp

TL;DR: An NH2-terminal fragment of mutant huntingtin was localized to neuronal intranuclear inclusions and dystrophic neurites in the HD cortex and striatum, and polyglutamine length influenced the extent of huntingtin accumulation in these structures.

TL;DR: Immunohistochemistry in human and rat brain revealed widespread cytoplasmic labeling of huntingtin within neurons, rather than the more selective pattern of axon terminal labeling characteristic of many vesicle-associated proteins.

TL;DR: The huntingtin-enriched cytoplasmic vacuoles formed in vitro internalized the lysosomal enzyme cathepsin D in proportion to the polyglutamine-length in huntingtin, which contributes to huntingtin proteolysis and to an autophagic process of cell death.

TL;DR: The early and proximate association of activated microglia with degenerating neurons in the HD brain implicates a role for activatedmicroglia in HD pathogenesis.

TL;DR: High-resolution lipidomic and proteomic analyses of exosomes and MVs derived by differential ultracentrifugation from 3 different cell types: U87 glioblastoma cells, Huh7 hepatocellular carcinoma cells and human bone marrow-derived mesenchymal stem cells are reported.