Alzheimer’s disease might be considered simply a series of pathways of progression in terms of a generic form of pathobiology that is specific to the genomic constitution of the individual patient suffering from the organic dementia.  Even in terms of such a paradoxically dual system of influence, however, the central attributes of brain atrophy as a neurodegenerative state might constitute genomic participation beyond a simple concept of selective neuronal susceptibility.  Indeed, one might speak of a generic series of steps that determines pathobiologic progression in neurons once injured, and that subsequent evolution to neurodegeneration and neuronal cell death is simply a consequence of such pathobiologic progression versus non-progression.  However, in real terms, also, one would perhaps realize a system that is generic in progression but characterized strictly by a genomic constitution that would itself be developmentally a chief determinant in a neurodegeneration as focal lesions of global distribution. Neuronal degeneration and neuronal cell death pathways would perhaps constitute an organic dementia of Alzheimer type largely as a genomic characterization of pathobiologic pathways of progression of neurons injured in potentially multiple different ways ranging from neuroinflammation to associated oxidative injury and vascular ischemia to forms of lipid peroxidation and catabolism.