1. 16- CYTOSKELETON

68. The gradual loss of brain function that characterizes
Alzheimer's disease seems to be due to two main forms of
nerve damage:
Nerve fibers grow tangled (neurofibrillary tangles)
protein deposits known as plaques build up in the brain

70. Amyloid plaques and neurofibrillary tangles (NFT)

71. Alzheimer's Disease is characterized by the formation of beta-amyloid plaques, as shown
here. Senile plaques appear as small collections of dark, irregular, thread-like structures
often with a brownish material in the center. The central core is represented by amyloid
and the irregular, beaded linear structures represent abnormal neurites (small dendrites
and axons with degenerative changes). However, tt has been hypothesized that the most
dangerous form beta-amyloid may be smaller groups of a few pieces, rather than the large
plaques themselves. The small clumps are suggested to synapse signaling and possible
trigger immune system inflamation.

74. 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- secretase
enzymes.
In a healthy brain, these beta-amyloid fragments are
broken down and eliminated. However, in AD, these
sticky fragments accumulate and fold into hard, insolube
clumps/fibrils, forming plaques on the surface of the
neuron.