Novel Proteins in α-Synucleinopathies

Abstract

α-Synucleinopathies are a group of neurodegenerative disorders char- acterized by the presence of intracytoplasmic Lewy bodies in Parkinson’s dis- ease and dementia with Lewy bodies as well as glial cytoplasmic inclusions in multiple system atrophy. The main component of these inclusions is aggregated α-synuclein which supports a strong link between α-synuclein and disease patho- genesis. The mechanisms responsible for α-synuclein aggregation and subsequent degeneration are largely unknown. However, several factors have been shown to accelerate the aggregation of α-synuclein in vitro and suggested to contribute to the pathogenesis of α-synucleinopathies. Several different proteins can stimulate the aggregation process in vitro and have been shown to colocalize with aggre- gated α-synuclein in pathological brain tissue. We review our current knowledge on proteins with a putative involvement in α-synuclein-dependent degeneration based on aggregatory properties, colocalization with aggregated α-synuclein, or genetic evidence.