Alzheimer's disease

Category B - full version without watermark 720x576 (check terms and conditions at The embed version with watermark is free of charge. Description: In the middle of the nineties genes, which are responsible for the Alzheimer disease, were discovered: presenilin 2 on chromosome 1 and presenilin 1 on chromosome 14 as well as mutations of the tau-gene on chromosome 19 and the amyloid-protein on chromosom 21 The modifications of the genetic sections of the on chromosomes lead to the typical increased sedimentation of plaque and go together with an early start of the alzheimer's disease. We know how the dramatic changes proceed - but we do not know why! The pathological process starts because of many different little malfunctions with the same result: the amyloid precurser protein APP - which is located on the membrane of the nerve cell is cut in a wrong way. Normally with the right cut harmless soluble left-overs would decay by itself - the wrong cut however creates fragments which agglomerate to neuro-toxic amyloid-lumps. Two enzymes are responsible for this fault: the beta-secretase and the gamma-secretase. In a healthy brain also these fragments would be distroyed whereas at Alzheimer's disease the fragments pile up to insoluble hard plaques with bad consequenses for the brain: the nervecells are put out of action. With a speciell developed marking process the beta amyloid-proteins can be made visible. The researchers hope to stop the formation of the B-amyloid in the future with new substances which will be able to block the responsiblet enzyme and so reduce the formation of plaque or avoide it totally. Alzheimer's disease attacks the brain; it is not a normal part of aging. People with AD have a gradual memory loss and difficulties with language and emotions. The progressive loss of intellectual abilities is termed dementia. The genetics of AD are confusing at best. Some families may have many members affected, but because family members may be exposed to the same environment, it is impossible to say how much heredity is to blame. Several genes have been identified on chromosomes 21 and 14 in the familial type of AD. In the more common sporadic type, people with a gene for a protein called apolipoprotein E on chromosome 19 tend to have a higher incidence of AD than the general population. Much more work needs to be done to fully understand how genetics influences the incidence of AD.