GBA1 and Parkinson disease: Here we show that defects in both autophagic and proteasomal pathways in a type II GD mouse model lead to accumulation of fragmented and bioenergetically compromised mitochondria in primary neurons and astrocytes lacking gba. Common hallmarks of neurodegeneration, including accumulation of ubiquitinated proteins and α-synuclein deposits found in PD, are also seen here in GD mouse brains.