Parkinson’s disease (PD) is a progressive neurodegenerative disorder resulting from the death of dopamine neurons in the substantia nigra pars compacta. Our understanding of PD biology has been enriched by the identification of genes involved in its rare, inheritable forms, termed PARK genes. These genes encode proteins including α-syn, LRRK2, VPS35, parkin, PINK1, and DJ1, which can cause monogenetic PD when mutated. Investigating the cellular functions of these proteins has been instrumental in identifying signaling pathways that mediate pathology in PD and neuroprotective mechanisms active during homeostatic and pathological conditions. It is now evident that many PD-associated proteins perform multiple functions in PD-associated signaling pathways in neurons. Furthermore, several PARK proteins contribute to non–cell-autonomous mechanisms of neuron death, such as neuroinflammation. A comprehensive understanding of cell-autonomous and non–cell-autonomous pathways involved in PD is essential for developing therapeutics that may slow or halt its progression.
The cell biology of Parkinson’s disease
P. Ge’s present address is Harvard–Massachusetts Institute of Technology MD/PhD Program, Harvard Medical School, Boston, MA; Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA; Picower Institute for Learning and Memory, Massachusetts Institute of Technology, Cambridge, MA; and Broad Institute of Massachusetts Institute of Technology and Harvard, Cambridge, MA.
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Nikhil Panicker, Preston Ge, Valina L. Dawson, Ted M. Dawson; The cell biology of Parkinson’s disease. J Cell Biol 5 April 2021; 220 (4): e202012095. doi: https://doi.org/10.1083/jcb.202012095
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