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Among these AD-associated pathologies, one deleterious effect that has attracted much attention in AD research is the downregulation of hippocampus-based neuroprotective molecules, especially BDNF (34)
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Previous work has established that any residual OCR detected after oligomycin A treatment is due to non-respiratory oxygen consumption, which is usually ascribed to proton leakage through the mitochondrial inner membrane 79
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