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.
