Revisiting the advance of age-dependent α-synuclein propagation and aggregation

Aging is a major risk factor for different neurodegenerative diseases (NDDs), including Parkinson’s disease (PD). In PD, one of the key neuropathological features is cytoplasmic protein aggregation, named Lewy bodies (LBs) in the cell body, and Lewy neurites (LNs) in neuronal processes and terminals. The protein α-synuclein (α-syn) has been found to be a major component of LBs and LNs, and is considered to play a central role in their formation. α-Syn also increases in healthy aging and in different disease conditions. Evidence has shown that aging promotes α-syn pathological aggregation and propagation and, therefore, may induce and aggravate PD pathogenesis. Here, we aim to highlight recent advances in age-related α-syn aggregation and prion-like propagation and discuss the subsequent consequences to neuronal functions.