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- W3049114493 abstract "Abstract Neurons are postmitotic cells of long duration and therefore strongly dependent on intracellular quality control mechanisms, such as the autophagic pathway, to maintain their homeostasis. Autophagy, first described as a process primarily inducible by starvation, is an intracellular pathway that promotes the degradation of damaged organelles, pathogens, and protein aggregates. Much evidence associates mitochondrial and lysosomal dysfunction as well as protein misfolding in the etiopathogenesis of Parkinson's disease (PD), indicating that alterations in the autophagic pathway that promote the accumulation of toxic protein aggregates and dysfunctional organelles, such as mitochondria, may contribute to the PD neurodegenerative process. In this chapter we will review studies that clearly show that the autophagic pathway is compromised in PD as well as discuss which signaling autophagic pathways are altered and identify autophagic targets and modulators that may be used as future strategies for the disease." @default.
- W3049114493 created "2020-08-21" @default.
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- W3049114493 date "2020-01-01" @default.
- W3049114493 modified "2023-09-27" @default.
- W3049114493 title "The role of autophagy in Parkinson's disease etiopathogenesis" @default.
- W3049114493 doi "https://doi.org/10.1016/b978-0-12-815950-7.00007-2" @default.
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