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Neuroimmunomodulation 2012

This also raises the question whether PARP activity in BRCA1/2-deficient tumors produces a similar metabolic phenotype via NAD + depletion and whether the use of a PARP inhibitor (e.g., olaparib) to treat these tumors 10 might restore NAD + levels and counterbalance GAPDH inhibition by other oxidative agents

Higher mitochondrial metabolism in the neurons result in generation of Complex I dependent hydrogen peroxide and neuronal membranes, rich in polyunsaturated fatty acids, are particularly vulnerable to oxidative stress due to their possession of unsaturated double bonds

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