There is an accumulation of extracellular neuritic plaques that have a core of amyloid beta proteins, intraneuronal neurofiblrillary tangles and degeneration of basal forebrain cholinergic neurons with loss of acetylcholine. The AD patient is unable to process and clear the mayloid precursor protein and results in an accumilation of toxic fragments of amyloid beta proteins that form diffuse neuritic plaques that disrupt nerve impulse transmission and cause death of the neuron.
A microtubule binding protein, tau protein, detatches and forms an insoluble filament called a neurofibrillary tangle that contribute to neuronal death. both the neuritic plaques and neurofrillary tangles become concentrated in the cerebral cortex and hippocampus. loss of neurons cause brain atrophy by widening of sulci and shrinkage of gyri. the decline of memory, loss of attention, and other cognitive functions are a result of a loss of synapses, acetylcholine and other neurotransmitters.