Acetylcholine and serotonin brain neurons can degenerate {Alzheimer's disease} {Alzheimer disease}, with intracellular tangled protein fibers {neurofibrillary tangle} and extracellular protein amyloid plaques.
plaque
Amyloid plaques can disrupt calcium regulation, create free radicals, or attract microglia. Presenilin gene makes gamma-secretase, which cuts cell-membrane protein {amyloid-beta precursor protein} (APP) inside membranes, and beta-secretase {secretase} cuts APP outside membranes, to make short A-beta proteins, which can be signal proteins. A-beta proteins can link hydrophobic ends to form plaques. Apolipoprotein E {apolipoprotein} (APOE-4) helps A-beta protein form plaques and slows A-beta protein removal. APP gene is on chromosome 21.
incidence
In USA, five million people have Alzheimer's disease. At age 60, 1 in 10,000 people develops Alzheimer's disease. By age 85, one in three people have dementia, typically Alzheimer's disease.
causes
Gene {presenilin gene} mutations can cause early-onset inherited Alzheimer's disease.
Apolipoprotein-E-gene isotype can modulate familial and sporadic Alzheimer's disease onset age.
Proteins {tau protein} can bind to tubulin, change, and increase in Alzheimer's disease. Tau proteins then make helical pairs, disrupting tubulin binding and microtubules.
Small proteins {amyloid beta-derived diffusible ligand} (ADDL) can come from amyloid-beta precursor proteins, can diffuse, do not make plaques, and attach to neuron receptors.
Brain proteins {clusterin} can increase in Alzheimer's disease.
Biological Sciences>Medicine>Disease>Kinds>Organ>Nerve>Aging
4-Medicine-Disease-Kinds-Organ-Nerve-Aging
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Date Modified: 2022.0224