In the beginning..

Article Abstract:

For years, circumstantial evidence has been accumulating to implicate beta amyloid in the pathogenesis of Alzheimer's disease (AD). Pathologists have long recognized that the development of amyloid plaques in the brain is a hallmark of AD, but it is virtually impossible to distinguish cause from effect simply by examining tissues at autopsy. However, in some families in which Alzheimer's disease is inherited as a dominant trait, a mutation has been found in the beta-amyloid precursor protein (beta-APP), suggesting that this protein is indeed directly involved in the development of the disorder. In the December 12, 1991 issue of Nature, scientists provide new evidence that beta-amyloid can cause degenerative neurological disease. The researchers used genetic engineering to develop laboratory mice that express a fragment of beta-APP in their brain cells. As these mice grow, pathological features develop that are strongly reminiscent of the changes observed in human Alzheimer's patients. This may prove to be the most successful animal model of AD to date. Such transgenic mice may also help researchers understand some of the effects of normal aging. Human beings, as well as a few other animals such as monkeys, accumulate amyloid beta/A4 protein in their brains. These accumulations have been termed ''preamyloid'' or ''diffuse'' plaques. In patients with Alzheimer's disease, such diffuse plaques are more common, and some apparently progress to a more compact form that is associated with pathological changes in the nerve fibers themselves. Alzheimer's disease may, therefore, not be distinct from the processes of normal aging, but may rather be an excessive expression of some normal aging processes. (Consumer Summary produced by Reliance Medical Information, Inc.)

Models

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Missense on the membrane

Article Abstract:

The development of Alzheimer's disease (AD) is associated with two genes, one present on chromosome 21 and the other on chromosome 19. Missense mutations in the beta-amyloid-precursor-protein gene, which favor production of the potentially neurotoxic A-beta fragment by the gene, cause the late-onset form of AD. A study conducted on fourteen early-onset familial AD pedigrees has identified the S182 gene, which contains five nucleotide changes in the amino-acid sequence in all the affected and some of the at-risk members of the family but not in normal subjects nor obligate escapees. The S182 protein has been identified as an integral membrane protein in which mutations may be linked to AD development.

Health aspects, Research, Causes of, Chromosome mapping, Mutation (Biology), Mutation

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Amyloid precursor on the G-O

Article Abstract:

Extracellular plaques made up of the peptide beta-amyloid found in the brains of people with Alzheimer's disease may be related to the disease symptomatically rather than causally. Ikuo Nishimoto and colleagues suggest that beta-amyloid precursor protein (APP), which gives rise to beta-amyloid, may also cause the plaques to form by controlling the heterotrimeric GTP-binding protein, G-O. However, APP's effect on other G proteins must be more fully assessed before this hypothesis can be accepted.

Physiological aspects, Development and progression, Peptides, Polypeptides

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