Abstract
The normal function of α-synuclein (α-syn) remains elusive. Although recent studies suggest α-syn as a physiologic attenuator of synaptic vesicle (SV) recycling, mechanisms are unclear. Here, we show that synapsin—a cytosolic protein with known roles in SV mobilization and clustering—is required for presynaptic functions of α-syn. Our data offer a critical missing link and advocate a model where α-syn and synapsin cooperate to cluster SVs and attenuate recycling.
Funder
HHS | NIH | National Institute on Aging
Israel Science Foundation
Publisher
Proceedings of the National Academy of Sciences
Cited by
81 articles.
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