Alzheimer's disease (AD) is characterized by a progressive cognitive decline associated with accumulation of ²-amyloid peptide (neuritic plaques), hyperphosphorylated tau protein (neurofibrillary tangles), synaptic degeneration and neuronal death in the hippocampus and other cortical regions. Studies have found that AD has a hypometabolism and a compromised mitochondrial bioenergetics, associated with increased oxidative stress. Recently, it has been observed that neurons can undergo a shift in metabolic profile, with the change of mitochondrial respiration (oxidative phosphorilation) to a profile of aerobic glycolysis as a compensatory mechanism for the production of energy and intermediary metabolites required for biomass, beyond the reduction of oxidative stress. However, the molecular mechanisms that underlie this metabolic exchange in nervous cells are poorly understood and have not been studied in subjects with the neuropathology of AD, but no evidence of cognitive impairment (DA asymptomatic). Thus, this study intends to investigate whether there are differences between subjects with symptomatic and asymptomatic DA and normal individuals in relation to energy metabolism.
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