For example, glutamatergic neurons expressing higher levels of endogenous α-syn are especially vulnerable to α-syn accumulation.246–250 Further, glutamatergic neurons express lower levels of BAG3, which is involved in autophagy.251 Lower BAG3 expression may lead to reduced α-syn degradation, in turn leading to increased accumulation.252 Additionally, in the α-syn seeding model of prodromal Parkinson’s disease, glutamatergic neurons exhibit Math2+ loss, a transcription factor underlying regulating mitochondrial homeostasis. This evidence concerns the gene NEUROD6 and Parkinson disease.