Selective vulnerability of neurons and selective resistance to neuronal injury appear to operate as pathways inducing functional or dysfunctional recovery in terms of both constitutive and acquired cellular attributes. Normal brain aging may transform to an Alzheimer type progression that induces acceleration of brain atrophy and also the emergence of specific lesions that range from neurofibrillary tangles to neuritic plaques. Neuronal cell loss may be apoptotic in terms of developmental origin of the cells or else involve neurodegenerative atrophy that culminates in variably expressed neuronal cell loss. Defining a distinction between successful brain aging and an Alzheimer disease process might specifically call into focus a series of neurodegenerative pathway effects that range from developmental to pathologic cell loss in determining transformation of cell atrophy to either programmed cell death or necrosis of neurons. A concept of increased susceptibility of select groups of neurons to neurofibrillary tangle formation and evolving neuritic plaques would call into question any reference to Alzheimer’s disease as a basic neurodegenerative event in the depletion of both hippocampal and cortical neuronal networks. There might arise a strictly determined focus of evolving change in neuronal homeostatic systems related primarily to how neurons deal with injurious events such as hypoxia or ischemia or even to varying systems of reactive recovery to hypoglycemia or deprived trophic effect. Alzheimer’s disease would progress as apoptosis beyond simple realized pathways of involved participation in cell injury. A role for apoptotic neuronal cell death might specifically implicate cell death pathways as a resolved means of compensatory recovery of neuronal networks that integrally are operatively functional or dysfunctional. In terms of such variability in cell response to injury, Alzheimer’s disease might prove a means of attempted recovery from injury inherent to an interaction of ischemic hypoxia and variable trophic factor deficit.