Getting in charge of β-synuclein fibrillation

The synuclein family has long been associated with Parkinson’s disease and dementia. Although the self-assembly of α-synuclein (αS) into oligomers and amyloid fibrils is well established, the aggregation propensity of other members of the family and their role in disease is still under debate. Moriarty et al. now suggest that the pH switching that occurs between different cellular environments could control β-synuclein (βS) aggregation via altering its charge distribution, thus opening new possible roles for βS in Parkinson’s and other neurodegen-erative diseases.