A schematic outline of progression of Alzheimer`s disease would implicate a neurodegenerative process arising from and sustained by various pathways of possible reactivity to neuronal injury. An etiologically operative system of pathogenic progression might simply evolve in terms of dysfunctionally variable trafficking systems, as phosphorylated Tau isoforms and of interactivity between the endoplasmic reticulum and Golgi subcompartments. Presenilins 1 and 2 might constitute a generic process of homology in molecular protein synthesis that primarily characterizes dysfunctionality of neurons in Alzheimer`s disease. A variability of response on the part of neuronal networks might help account for subsequent progression of a clinically demented state characterized by microscopic parameters of accumulation of neurofibrillary tangles and neuritic plaques and of amyloidogenesis. Lewy body accumulation as an inclusion body disease affecting extrapyramidal system and cortical neurons might participate in such neuronal network involvement.