Margaret M.P. Pearce

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

This study shows that mutant huntingtin aggregates impair glial phagocytosis and phagolysosomal function in Drosophila, leading to prion-like propagation of aggregates and neurodegeneration.

Phagocytic glia are obligatory intermediates in transmission of mutant huntingtin aggregates across neuronal synapses

The paper shows that mutant huntingtin aggregates spread between neurons via phagocytic glia in Drosophila, requiring the Draper receptor and synaptic dysfunction.