Journal
CELLS
Volume 9, Issue 1, Pages -Publisher
MDPI
DOI: 10.3390/cells9010233
Keywords
alpha-syn; LRRK2; DJ-1; Parkin; PINK1; ATP13A2; VPS35; MAM; mitophagy; neurodegeneration
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Funding
- Bangerter-Rhyner Foundation
- Mach-Gaensslen Foundation
- Novartis Foundation for medical-biological Research [18C194]
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The pathogenesis of Parkinson's disease (PD), the second most common neurodegenerative disorder, is complex and involves the impairment of crucial intracellular physiological processes. Importantly, in addition to abnormal alpha-synuclein aggregation, the dysfunction of various mitochondria-dependent processes has been prominently implicated in PD pathogenesis. Besides the long-known loss of the organelles' bioenergetics function resulting in diminished ATP synthesis, more recent studies in the field have increasingly focused on compromised mitochondrial quality control as well as impaired biochemical processes specifically localized to ER-mitochondria interfaces (such as lipid biosynthesis and calcium homeostasis). In this review, we will discuss how dysregulated mitochondrial crosstalk with other organelles contributes to PD pathogenesis.
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