PSYC 2240 Chapter 12&14: PSYCH 2240 Chapters 12& 14 Test 3 Nov 25
22 Nov 2014
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About half of all patients with late-onset alzheimer"s disease have no known relatives with the disease. : genes controlling early onset cause this protein to accumulate both inside. The impact varies among cells but he net effect is to damage dendritic spines, decrease synaptic input and decrease plasticity. Amyloid damages axons and dendrites, the damage structures cluster into structures called plaques. As the plaques accumulate the cerebral cortex, hippocampus and other areas atrophy (waste away). Tau protein: a second problem in the intracellular support structure of axons. High levels of amyloid cause more phosphate groups to attach to tau proteins. The alter tau can"t bid to its usual targets within axons, and so it starts spreading into the cell body and dendrites. The attack of tau from within dendrites adds to the attack by amyloid b, magnifying the damage. Researchers hypothesize that altered tau also increases production of amyloid b causing a vicious cycle.
