Genes that can cause neurofibrillary tangles and amyloid plaques are strongly associated with Alzheimer's disease.

Much of the research relating to Alzheimer's genes focuses on neurofibrillary tangles and amyloid plaques, both of which are associated with memory loss by blocking synapse function. Tangles are thin, twisted bundles of protein inside neurons, which can result from mutations in the tau protein. Amyloid plaques are clumps of proteins that accumulate in the brains of Alzheimer's patients. Genes responsible for the formation of amyloid plaques can be understood in terms of three interacting groups: 1) Increased production of amyloid protein: Mutations in the APP gene, PS1 gene, or PS2 gene can lead to the production of too much amyloid protein. These genes are particularly associated with early-onset Alzheimer's. 2) Accelerated plaque formation of amyloid protein: The APOE gene has a number of different isoforms (APOE2, APOE3, and APOE4). APOE4 binds rapidly to beta amyloid, which may lead to excess retention in the brain. 3) Decreased clearing of amyloid protein: A third gene group consisting of many candidate genes may be involved in removing amyloid build-up. Failure to remove amyloid from the brain may also lead to an eventual build up of the protein. These three causal mechanisms for Alzheimer's can interact with one other. For example, combining excessive production of amyloid with an impairment in removing build-up of the protein could increase the probability of developing Alzheimer’s.

alzheimer, alzheimer's disease, candidate genes, beta amyloid, amyloid, neurofibrillary tangles, tau protein, APP, apoe, apoe4, tau, ps1, ps2, psen1, psen2, presenilin