Induced progression of a whole heterogeneous series of apoptotic pathways involved in various forms of neurodegeneration ranging from clinical dementia to selective neuronal subset depletion would implicate a realized form of evolving injury to nucleus and cell organelles such as mitochondria. Windows of susceptibility in the development of such injury might allow for the development of pathways of promoted transformation as best depicted in age-related dementia of possibly multifactorial type. One might indeed recognize dynamics of nuclear and mitochondrial membrane injuries that allow for further delineation of factors of evolving change that globally participate in subsequent progression. Etiologic and pathogenetic involvement of injury in the precipitation of apoptotic pathways might allow for a redefinition of injury to cells beyond simple concepts of induced effect. Moreover, progression might indeed allow for the subsequent delineation of events as borne out by the clearly defined schemes of prototypical events evidenced morphologically in terms of Alzheimer-type neurodegeneration or in the synucleinopathy of Idiopathic Parkinson’s disease.