Abstract
Reduced complex IV, increased oxidative stress and beta amyloid peptide secretion in Alzheimer's disease (AD) can be replicated in cybrid models. We characterized cyclical mitochondrial ΔΨ M fluctuations (‘flickering’) in neuroblastoma cells and AD/CTL cybrids. Flickering was blocked by ATP-synthase inhibition, was not observed in rho 0 cells and was not blocked by antioxidant treatment. Flickering was not affected by the Ca +2 uniporter antagonist Ru360 but was eliminated by BAPTA or CGP37137 blockade of the mitochondrial Na +/Ca +2 exchanger. AD cybrid mitochondria showed reduced flickering. Flickering seems to represent coupling of ΔΨ M to F 0F 1 ATP-synthase; reduction of flickering in AD cybrids suggests dysfunction of this coupling.
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