Figure 8.
The multi-functional role of endophilin-B1 in Alzheimer’s disease pathogenesis. Amyloid-β accumulation leads to decreased endophilin-B1b/c expression in neurons, which in turn elevates amyloid-β and plaques, possibly through impairment of autophagy. Loss of endophilin-B1b/c may concomitantly increase neuronal vulnerability to amyloid-β toxicity through its potential function in synapses and mitochondria.