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- W4283121266 endingPage "6808" @default.
- W4283121266 startingPage "6808" @default.
- W4283121266 abstract "Parkinson's disease is a neurodegenerative condition initially characterized by the presence of tremor, muscle stiffness and impaired balance, with the deposition of insoluble protein aggregates in Lewy's Bodies the histopathological hallmark of the disease. Although different gene variants are linked to Parkinson disease, mutations in the Leucine-Rich Repeat Kinase 2 (LRRK2) gene are one of the most frequent causes of Parkinson's disease related to genetic mutations. LRRK2 toxicity has been mainly explained by an increase in kinase activity, but alternative mechanisms have emerged as underlying causes for Parkinson's disease, such as the imbalance in LRRK2 homeostasis and the involvement of LRRK2 in aggregation and spreading of α-synuclein toxicity. In this review, we recapitulate the main LRRK2 pathological mutations that contribute to Parkinson's disease and the different cellular and therapeutic strategies devised to correct LRRK2 homeostasis. In this review, we describe the main cellular control mechanisms that regulate LRRK2 folding and aggregation, such as the chaperone network and the protein-clearing pathways such as the ubiquitin-proteasome system and the autophagic-lysosomal pathway. We will also address the more relevant strategies to modulate neurodegeneration in Parkinson's disease through the regulation of LRRK2, using small molecules or LRRK2 silencing." @default.
- W4283121266 created "2022-06-20" @default.
- W4283121266 creator A5010963305 @default.
- W4283121266 creator A5052379250 @default.
- W4283121266 creator A5066899595 @default.
- W4283121266 creator A5088274147 @default.
- W4283121266 date "2022-06-18" @default.
- W4283121266 modified "2023-09-25" @default.
- W4283121266 title "LRRK2 and Proteostasis in Parkinson’s Disease" @default.
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