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- W2896586855 abstract "Parkinson disease (PD) is a progressive neurological disease caused by selective degeneration of dopaminergic (DA) neurons in the substantia nigra. Although most cases of PD are sporadic cases, familial PD provides a versatile research model for basic mechanistic insights into the pathogenesis of PD. In this study, we generated DA neurons from PARK2 patient-specific, isogenic PARK2 null and PARK6 patient-specific induced pluripotent stem cells and found that these neurons exhibited more apoptosis and greater susceptibility to rotenone-induced mitochondrial stress. From phenotypic screening with an FDA-approved drug library, one voltage-gated calcium channel antagonist, benidipine, was found to suppress rotenone-induced apoptosis. Furthermore, we demonstrated the dysregulation of calcium homeostasis and increased susceptibility to rotenone-induced stress in PD, which is prevented by T-type calcium channel knockdown or antagonists. These findings suggest that calcium homeostasis in DA neurons might be a useful target for developing new drugs for PD patients." @default.
- W2896586855 created "2018-10-26" @default.
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- W2896586855 date "2018-11-01" @default.
- W2896586855 modified "2023-10-17" @default.
- W2896586855 title "T-type Calcium Channels Determine the Vulnerability of Dopaminergic Neurons to Mitochondrial Stress in Familial Parkinson Disease" @default.
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- W2896586855 doi "https://doi.org/10.1016/j.stemcr.2018.09.006" @default.
- W2896586855 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6234903" @default.
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