The gradual loss of brain function that characterizesAlzheimers disease seems to be due to two main forms ofnerve damage:Nerve fibers grow tangled (neurofibrillary tangles)protein deposits known as plaques build up in the brain
Amyloid plaques and neurofibrillary tangles (NFT)
Alzheimers Disease is characterized by the formation of beta-amyloid plaques, as shownhere. Senile plaques appear as small collections of dark, irregular, thread-like structuresoften with a brownish material in the center. The central core is represented by amyloidand the irregular, beaded linear structures represent abnormal neurites (small dendritesand axons with degenerative changes). However, tt has been hypothesized that the mostdangerous form beta-amyloid may be smaller groups of a few pieces, rather than the largeplaques themselves. The small clumps are suggested to synapse signaling and possibletrigger immune system inflamation.
Beta-amyloid is a fragment of a protein that is snipped from amyloid precursor protein (APP), a surface protein produced by healthy cells. Much is still unknown about APP, such as its precise role in normal physiology. Many possibilities have been reported. It has been suggested that APP may be a receptor, and/or that it may serve as a link between kinesin molecular motors and synaptic vesicles. Roles as an adhesion protein, and a function relating to promotion of neurite growth have also been proposed. Gene transcriptional activity has been attributed to APP as well.Beta-amyloid is cleaved by beta- and gamma- secretaseenzymes.In a healthy brain, these beta-amyloid fragments arebroken down and eliminated. However, in AD, thesesticky fragments accumulate and fold into hard, insolubeclumps/fibrils, forming plaques on the surface of theneuron.