Impacts of increased α-synuclein on clathrin-mediated endocytosis at synapses:implications for neurodegenerative diseases
Audrey T. Medeiros
Luigi Bubacco
Jennifer R. Morgan
摘要：α-Synuclein causes synaptic pathologies in several neurodegen-erative 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 pro-tein that normally associates with synaptic vesicle membranes and regulates synaptic vesicle trafficking under physiological conditions (Calo et al., 2016). 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, al-though other brain areas are also affected (Schulz-Schaeffer, 2010).
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资助基金：This research was supported by a grant from National Institutes of Health(NINDS/NIA R01NS078165 to JRM)
论文发表日期：2018-01-01
在线出版日期：2025-08-15（本平台首次上网日期，不代表文献的发表时间）
页数：2( 647-648 )