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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 neurodegenerative diseases. © 2017 by The American Society for Biochemistry and Molecular Biology, Inc.

Citation

Meytal Landau. Getting in charge of β-synuclein fibrillation. The Journal of biological chemistry. 2017 Sep 29;292(39):16380-16381

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PMID: 28963338

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