The pathological features of Alzheimer's disease include the presence of p-amyloid plaques, T-enriched neurofib-rillary tangles, neuronal loss, and alterations in many neu-rotransmitter systems. Affected brain regions include the entorhinal cortex; hippocampus; amygdala; association cortices of the frontal, temporal and parietal lobes; and subcortical nuclei that project to these regions. Characteristically, the brains of Alzheimer's disease patients contain two distinct types of insoluble materials that are hallmarks of the brain lesions associated with the disorder: extracellular neuritic plaques containing p-amyloid (Ap) and intracellular T-enriched neurofibrillary tangles. As with Lewy bodies in Parkinson's disease, it is unclear whether the tangles and plaques are causal or byproducts of degenerative processes. However, considerable evidence suggests that alterations in Ap processing may be necessary components of cell destruction.

One theory of the pathogenesis of Alzheimer's disease proposes that increased production or decreased secretion of the Ap peptides leads to accumulation of these peptides. A second theory proposes that an abnormal T-protein causes the formation of intracellular neu-rofibrillary tangles. T-Proteins are important in the maintenance of cytoskeleton function and axonal transport of proteins. Another theory is that Ap accumulation is a precipitating factor that is followed by the development of the T-enriched tangles in the dying neurons.

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