It proposed that, the energy requirements of the AD brain might be compromised by the decrease in NADH synthesis consequent upon a decline in TPI catalytic activity caused by excessive glycolytic activity in the brain, plus the effects of accumulation of certain aberrant protein molecules (beta-amyloid peptide-induced nitration of TPI and loss of tau-mediated TPI protection). The gene discussed is TPI1; the disease is Alzheimer disease.