Impairment of the glial phagolysosomal system drives prion-like propagation in a Drosophila model of Huntington's disease.

model of Huntington's disease that neuronal mHTT aggregates interfere with glial phagocytic engulfment, phagolysosomal processing, and innate immunity transcriptional responses. We also identify Rab10 as a novel modifier of prion-like transmission of mHTT aggregates. Our findings add to a growing narrative of glia as double-edged players in neurodegenerative diseases.