Loss of Synaptically Determined Viability of Neurons in Alzheimer Brain Atrophy

Multiple exogenously derived systems of promotion and of induced progression would perhaps actually participate within contextual frameworks of self-promotion as age-related dementia. Indeed, impaired synaptic connectivity and impaired synaptic integrity might assume pathogenic roles leading to aspects of both induced and self-promotion towards pathways of evolving brain atrophy. Even beyond simple schemes of induced effect or of self-progression, however, synaptic transmission or non-transmission might help characterize the Alzheimer process as systems of disturbance arising from micro-circulatory ischemia to lack of neurotrophic effect to systems of nonviability of neurons and of neuronal non-responsiveness. In simple terms, the specific associations of the Alzheimer process with aging would appear a specific characterization of synaptic pathobiology central to basic dynamics of dementia both as an organic atrophic state and also as persistently active pathways of progression once initiated.