Post-translational modification of α-synuclein in Parkinson׳s disease

Abstract

Parkinson׳s disease (PD) is the second most common neurodegenerative disease, and the most prevalent degenerative movement disorder. It is estimated that the prevalence of such age-related neurodegenerative diseases will double in the next 25 years. While the etiology of Parkinson׳s disease is not entirely clear, a common link between both inherited and sporadic forms of disease is the protein α-synuclein. In PD brains, α-synuclein is typically found in large, insoluble protein aggregates referred to as Lewy bodies and Lewy neurites. The exact role of α-synuclein is still unknown, but it has been shown to undergo a variety of post-translational modifications, which impact α-synuclein aggregation and oligomer formation in different ways. This review highlights key post-translational modifications and the impact they have on α-synuclein aggregation and toxicity, elucidating potential mechanisms for PD pathogenesis and targets for future therapeutics.This article is part of a Special Issue entitled SI: Neuroprotection.