Neural Regeneration Research ›› 2018, Vol. 13 ›› Issue (4): 647-648.doi: 10.4103/1673-5374.230289

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Impacts of increased α-synuclein on clathrin-mediated endocytosis at synapses: implications for neurodegenerative diseases

Audrey T. Medeiros1, Luigi Bubacco2, Jennifer R. Morgan1   

  1. 1 The Eugene Bell Center for Regenerative Biology and Tissue Engineering, Marine Biological Laboratory, Woods Hole, MA, USA;
    2 Department of Biology, University of Padova. Padova, Italy
  • Received:2018-03-07 Online:2018-04-15 Published:2018-04-15
  • Contact: Jennifer R. Morgan, Ph.D., jmorgan@mbl.edu
  • Supported by:

    This research was supported by a grant from National Institutes of Health (NINDS/NIA R01NS078165 to JRM), research funds from the MarineBiological Laboratory (to JRM), and a research grant from Horizon 2020 Grant No. InCure EU Joint Programme-JPND (to LB).
    This research was presented in American Society for Cell Biology in December  2016 and in Society for Neuroscience in November 2017.

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Abstract:

α-Synuclein causes synaptic pathologies in several neurodegenerative diseases: Parkinson’s disease (PD) is a neurodegenerative disease that impacts the lives of millions of people worldwide. A pathological hallmark of PD, as well as dementia with Lewy bodies (DLB) and several Alzheimer’s disease variants, is the appearance of intracellular inclusions called Lewy bodies, which contain high levels of aggregated α-synuclein. α-Synuclein is a presynaptic protein that normally associates with synaptic vesicle membranes and regulates synaptic vesicle trafficking under physiological conditions . However, in familial PD, multiplication and several point mutations in the α-synuclein gene (SNCA) ultimately lead to toxic aggregation of the α-synuclein protein and subsequent degeneration of dopaminergic neurons in the substantia nigra, although other brain areas are also affected .