Abstract: Set patterns of evolution of the Alzheimer’s disease process might follow systems of reactivity in response to injury affecting multiple neuronal suborganelles. This may be conducive to the creation of programmed events as individual cell loss or neuronal dropout. The neuronal plasmalemma and other membranous cell components, would lead to the generation of progressive cascade-like events in neuronal depletion and brain atrophy. Selective vulnerability of neurons might specifically implicate pathobiologic processes that affect responsive elements in progression of the injury. Such injury appears based on integrative pathways induced especially by trophic factor insufficiency and vascular hypoperfusion. Alzheimer’s disease appears to evolve as compromised recoverability of neurons that further delineate susceptibility patterns of neuronal subsets. Indeed, the neuronal pathobiology in Alzheimer’s disease would center on aberrant modes of reactivity to a host of potential injurious agents that subsequently may evolve as programmed neuronal cell loss. Such cell loss would primarily arise on an individual neuronal cell basis and subsequently develop into aggregate loss of network connectivity.