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- W2033202184 abstract "Mitochondrial dysfunction has been implied in Parkinson's disease (PD) leading to neuronal death. Alpha-synuclein aggregations have been shown to be a pathological hallmark in PD patients. This current study investigates a possible effect of alpha-synuclein on mitochondrial health.We have used fluorescence imaging and TMRM to measure the mitochondrial membrane potential (Δψm) in mouse primary co-cultures of neurons and astrocytes and human iPS derived neurons.Human iPS derived neurons bearing a triplication of the alpha-synuclein gene displayed a significantly lower Δψm (61.4±3.9% of control). Importantly, basal Δψm in alpha-synuclein overexpressing cells was dependent on the age of cells which possibly reflects an increase in expression levels of alpha-synuclein.Application of oligomycin to alpha-synuclein overexpressing neurons induced a mitochondrial depolarisation, suggesting that Δψm is partially maintained through the hydrolysis of ATP by F1F0-ATPases due to an impaired mitochondrial respiration.The current study found also that the stimulation of TMRM-loaded human neurons with a high laser power (565 nm) produced ROS and induced a rapid drop in Δψm which can be partially rescued by a pre-incubation with an inhibitor of the permeability transition pore (PTP) cyclosporine A. The ROS-induced PTP opening appeared much faster in human alpha-synuclein overexpressing neurons when compared to control neurons. Additionally, application of the same method to primary neuronal mouse cultures demonstrated that pre-incubation of these cells with monomeric or oligomeric alpha-synuclein induced significantly faster PTP opening.This work was supported by the MRC and Wellcome Trust." @default.
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- W2033202184 date "2014-01-01" @default.
- W2033202184 modified "2023-09-28" @default.
- W2033202184 title "Alpha-Synuclein Induces Mitochondrial Dysfunction Leading to a Higher Susceptibility of PTP Opening" @default.
- W2033202184 doi "https://doi.org/10.1016/j.bpj.2013.11.3269" @default.
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