2018, Number S1
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ABSTRACTBackground: Recent evidence suggests that early neurodegenerative events associated with Alzheimer’s disease (AD) probably begin in the synaptic terminal, where it has been reported a large accumulation of β-amyloid protein (Aβ), one of the main factors described in the development of AD. We analyzed the influence of energy metabolism on the toxic effects of Aβ during aging on synaptosomes from neocortex and hippocampus of rats exposed to inhibitors of glycolytic and mitochondrial metabolism and we evaluated the protective effects of some antioxidant compounds.
Methods: Synaptosomes were obtained by differential centrifugation in sucrose gradients and their redox activity was determined with the MTT assay.
Results: The mitochondrial activity of synaptosomes from young rats was not altered by the presence of Aβ; the ones obtained from old rats showed an increase in susceptibility to Aβ; this activity was greater in the synaptic terminals of the hippocampus.
Conclusions: These results provide experimental support for the hypothesis that certain risk factors, such as energy metabolism dysfunction or the aging process itself, may increase vulnerability to Aβ. Hippocampal region is more susceptible to Aβ and its effect increases with age in relation to the neocortex, which would agree with the damage gradient reported in the AD.
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