AD seems to be caused by the selective degeneration of neuronal populations.
Pathophysiologic studies done on Alzheimer brains postmortem show neurofibrillary tangles and senile plaques in the cerebral cortex and temporal lobe. We demonstrated a decrease in brain glucose uptake in vivo by positron emission tomography and by examining brain microvessels in AD patients. We also revealed that a key defect in AD is the decreased ability, via a decrease in the activity of the enzyme hexokinase, of the brain to utilize glucose as an energy source. Growing evidence exists of the participation of free-radical oxidative interactions in promoting tissue injury in neurodegenerative diseases such as Parkinson disease, multiple sclerosis, and Alzheimer disease. The cell unaffected by Alzheimer disease is longer, fuller, and spinier.