Abstract
Strict evolutionary principles would apply for the pathogenesis of both local and global pathway events in delineating lesions of Alzheimer type. It is further to be realized that the complex modulatory role of disease activity conforms to the advancement and propagation of a substrate susceptibility indicative of further cascade events in such evolution. Overall dimensions of expansion and contraction would perhaps account for the betaamyloid turnover events between the intracellular and extracellular compartments in a manner specifically inducive towards a complex constitution of atrophy and neuronal loss in the cerebral cortex. Synaptic compromise and the post-synaptic receptor apparatus would further indicate the development of subsidiary or secondary pathways that include a significant role for plasticity in lesion involvement.
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