期刊
SCIENCE
卷 358, 期 6369, 页码 1440-+出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.aan6160
关键词
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资金
- Parkinson's UK [G-1508]
- UK Medical Research Council [MR/N000676/1]
- Wellcome Trust [104933/2/14E]
- Leverhulme Trust [RPG-2015-350, RPG-2015-345]
- British Heart Foundation [PG/14/93/31237, PG/11/81/29130]
- UK Biotechnology and Biological Sciences Research Council [BB/M023923/1, BB/G00594X/1]
- Agency of Science, Technology and Research of Singapore
- Ministry of Economy, Industry, and Competitiveness of Spain [MINECO RYC-2012-12068, MINECO/FEDER EU BEU2015-64119-P]
- Regione Toscana (SUPREMAL)
- University of Florence (Eondi di Ateneo)
- Centre for Misfolding Diseases of the University of Cambridge
- Biotechnology and Biological Sciences Research Council [BB/M023923/1, BB/G00594X/1] Funding Source: researchfish
- British Heart Foundation [PG/11/81/29130, PG/14/93/31237] Funding Source: researchfish
- Medical Research Council [MR/N000676/1] Funding Source: researchfish
- Parkinson's UK [G-1508, H-1103] Funding Source: researchfish
- BBSRC [BB/G00594X/1, BB/M023923/1] Funding Source: UKRI
- MRC [MR/N000676/1] Funding Source: UKRI
Oligomeric species populated during the aggregation process of alpha-synuclein have been linked to neuronal impairment in Parkinson's disease and related neurodegenerative disorders. By using solution and solid-state nuclear magnetic resonance techniques in conjunction with other structural methods, we identified the fundamental characteristics that enable toxic alpha-synuclein oligomers to perturb biological membranes and disrupt cellular function; these include a highly lipophilic element that promotes strong membrane interactions and a structured region that inserts into lipid bilayers and disrupts their integrity. In support of these conclusions, mutations that target the region that promotes strong membrane interactions by alpha-synuclein oligomers suppressed their toxicity in neuroblastoma cells and primary cortical neurons.
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