Abstract:
:Parkinson's disease (PD) is a common neurodegenerative disease, yet the underlying causative molecular mechanisms are ill defined. Numerous observations based on drug studies and mutations in genes that cause PD point to a complex set of rather subtle mitochondrial defects that may be causative. Indeed, intensive investigation of these genes in model organisms has revealed roles in the electron transport chain, mitochondrial protein homeostasis, mitophagy, and the fusion and fission of mitochondria. Here, we attempt to synthesize results from experimental studies in diverse systems to define the precise function of these PD genes, as well as their interplay with other genes that affect mitochondrial function. We propose that subtle mitochondrial defects in combination with other insults trigger the onset and progression of disease, in both familial and idiopathic PD.
journal_name
Annu Rev Neuroscijournal_title
Annual review of neuroscienceauthors
Haelterman NA,Yoon WH,Sandoval H,Jaiswal M,Shulman JM,Bellen HJdoi
10.1146/annurev-neuro-071013-014317subject
Has Abstractpub_date
2014-01-01 00:00:00pages
137-59eissn
0147-006Xissn
1545-4126journal_volume
37pub_type
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