There is a reduction in cortical neuronal density with accompanying changes in cerebral blood flow with aging (Morgan et al. 2007, Prough 2005, Sadean and Glass 2003). Cerebral blood flow decreases by 10-20% in proportion to neuronal losses. This is largely attributed to increased apoptotic activity of cerebral neurons, particularly in the cerebral cortex and frontal lobes. Additionally, deranged cellular calcium homeostatic mechanisms cause altered synaptic activity and signal transduction. The number of synapses and their corresponding receptors are reduced [i.e., decreased serotonergic, adrenergic, and gamma-aminobutyric acid (GABA) binding sites]. There is also a reduction in neuronal regenerative capacity (Vuyk 2003). Additionally, N-methyl-D-acetate (NMDA) receptor-binding sites have been reported to decrease by 50% in aged animals (Vuyk 2003).
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