Abstract: Alzheimer disorders of neuritogenesis and of senile plaque formation are progressive in terms of a developmental predetermining series of steps in evolution of amyloidogenesis and of neuronal cell depletion and loss. Tissue atrophy of the cerebral cortex and white matter appear both integral aspects of a disease process that evolves to implicate microcirculatory and vascular wall pathology or impermeability. The extracellular dimensions of the senile plaque appear exquisitely sensitive to the conditioning and transforming influences of pathology of Alzheimer type. Neurofibrillary tangles and congophilic angiopathy and also the various other manifestations of Alzheimer brain atrophy include a particular association with neuritic dystrophy and dysfunctionality of synapses and of neuronal circuits. It might be particularly significant to recognize the Alzheimer disease process as one that inherently arises in consequence to a variety of associative factors that secondarily determine developmental progression of neuronal cell loss and of tissue atrophy. A central process of apoptosis as transformed dynamics of cell loss and of altered attributes of otherwise active maintenance of cell metabolic and physiologic pathways might account for a depletion that is genetically programmed but predominantly associated with acquired associative events of progression.