期刊
FRONTIERS IN CELLULAR NEUROSCIENCE
卷 16, 期 -, 页码 -出版社
FRONTIERS MEDIA SA
DOI: 10.3389/fncel.2022.1081426
关键词
Parkinson's disease; alpha-synuclein; endolysosomal; endocytosis; trafficking
Parkinson's disease (PD) is a chronic neurodegenerative disease characterized by loss of dopaminergic neurons. Protein trafficking and α-synuclein have been identified as major contributors to the death of these neurons. Recent research suggests that α-synuclein can propagate through the brain and form aggregates. Understanding the mechanisms of α-synuclein propagation and clearance is crucial for therapeutic strategies.
Parkinson's disease (PD) is a chronic neurodegenerative disease that is characterized by a loss of dopaminergic neurons in the substantia nigra pars compacta of the midbrain (SNpc). Extensive studies into genetic and cellular models of PD implicate protein trafficking as a prominent contributor to the death of these dopaminergic neurons. Considerable evidence also suggests the involvement of a-synuclein as a central component of the characteristic cell death in PD and it is a major structural constituent of proteinaceous inclusion bodies (Lewy bodies; LB). a-synuclein research has been a vital part of PD research in recent years, with newly discovered evidence suggesting that a-synuclein can propagate through the brain via prion-like mechanisms. Healthy cells can internalize toxic a-synuclein species and seed endogenous a-synuclein to form large, pathogenic aggregates and form LBs. A better understanding of how a-synuclein can propagate, enter and be cleared from the cell is vital for therapeutic strategies.
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