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- W2168021147 abstract "Although the pathogenesis of Parkinson's disease (PD) is considered multifactorial, evidence from genetics and cell biology has implicated specific molecular pathways. This article summarizes evidence that suggests that the level of intracellular alpha-synuclein is critical for the onset of neurodegeneration with Lewy bodies and dependent, to a large extent, on lysosomal degradation. The function of other key proteins that emerged from genetics is discussed: Pink1 and Parkin regulate the degradation of damaged mitochondria by the lysosome (mitophagy). Glucocerebrosidase and ATP13A2 are important components of this degradative organelle. VPS35 and LRRK2 may regulate trafficking within lysosome-dependent pathways, such as autophagy and endosomal vesicle recycling. Clinically, diffuse alpha-synucleinopathy or dementia seems to correlate with mutations which interfere with the broader function of lysosomal pathways, whereas a predominantly motor syndrome and nigrostriatal degeneration is associated with specific defects in mitophagy. Based on these studies, it is proposed that a protein network involved in trafficking to, or degradation by, lysosomes could be sufficient to explain the phenotypic spectrum within PD in a unifying biochemical pathway. © 2012 Movement Disorder Society" @default.
- W2168021147 created "2016-06-24" @default.
- W2168021147 creator A5067875688 @default.
- W2168021147 date "2012-08-23" @default.
- W2168021147 modified "2023-10-02" @default.
- W2168021147 title "Lysosome-dependent pathways as a unifying theme in Parkinson's disease" @default.
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- W2168021147 doi "https://doi.org/10.1002/mds.25136" @default.
- W2168021147 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/22927213" @default.
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