A self-progressive neurodegenerative event of Alzheimer type would involve a distinctive process of increasing membrane proteolysis as the cause of neuronal cell death and of various aberrant attempts at dystrophic recovery.  Indeed, a conceptual distinction of the Alzheimer process from senile brain atrophy might arise as a strict phenomenon of evolving protein-protein interactions and of various aberrant patterns of intracellular protein trafficking that mark out the Alzheimer neurodegenerative event as paradoxically both constitutional and possibly also of acquired nature.  In terms, indeed, of a progressive phenomenon of atrophy of the brain that is neuronal in specific pathogenesis but also arising inherently as a neurodegenerative series of aberrant pathway attempts at recovery of injured neurons, a single event of degeneration would arise from proteolytic involvement of the neuronal cell body. It is in terms of such a postulated integral event of self-progressive proteolysis arising and evolving within neuronal membranes that there would be implicated not only ApoE isoforms but also Presenilin-1 and –2 as membrane-anchored molecules of progression in the Alzheimer process. Indeed, an integral neurodegenerative event of neuronal membrane processing would arise and proceed as a series of synaptic and neuritic dystrophic forms of activity specifically distinguishing the disorder from simple senile brain atrophy.  It is perhaps in terms of quantitatively significant degrees of increased neuronal cell loss that Alzheimer disease would indeed constitute an active participation of various membrane-based transformations ranging from ubiquination to proteolysis to protein-protein interaction and lipid metabolism to Ca2 + /K + channeling as one constitutive Alzheimer process with added acquired dimensions.