Amyloid beta-protein deposition in tissues other than brain in Alzheimer's disease

Article Abstract:

Alzheimer's disease is characterized by the progressive loss of intellectual functioning in aging humans. In Alzheimer patients three types of lesions with a filamentous, or string-like, structure occur in three areas of the brain: neurofibrillary tangles within neurons or nerve cells; plaques made of the amyloid (beta)-protein, in extracellular deposits in the brain; and amyloid (beta)-protein deposits in blood vessels in the brain. Amyloid (beta)-protein is also found as filaments in plaques and blood vessels of the brain in normal aged individuals and in individuals with Down's syndrome, an inherited condition characterized by various degrees of mental retardation. These lesions had only been found in the brain. However, this report shows that deposits of amyloid protein are present in other non-neural tissues (which are outside of the nervous system) including blood vessels of the skin, subcutaneous tissues (tissues beneath the skin) and the intestines. In these areas the amyloid deposits are diffuse, but lesions with the filamentous structure do occur in some healthy, aging individuals. The amyloid (beta)-protein was detected with a very sensitive test using an antibody molecule, a protein of the immune system that specifically recognized amyloid (beta)-protein. Amyloid (beta)-protein may be produced locally in many organs or may be made from a precursor protein that is present in the blood circulation. If a circulating form of the amyloid molecule exists, new therapeutic approaches could be designed to prevent both the deposition of the amyloid protein in the brain and the symptoms of Alzheimer's disease.

Aging, Reports, Down syndrome, Protein research

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Amyloid beta-peptide is produced by cultured cells during normal metabolism

Article Abstract:

The amyloid beta-peptide (A-beta) fragment that is linked to Alzheimer's disease has been identified in 4K and truncated form from cultures of primary, untransfected and beta-amyloid precursor protein-transfected brain cells. The production of A-beta in soluble form in vitro and in vivo as a part of normal metabolism shows that existing concepts of Alzheimer's disease pathology must be re-evaluated. Moreover, the new knowledge of A-beta's functions may lead to drugs that prevent or treat Alzheimer's disease by stopping the secretion of A-beta.

Health aspects, Peptides

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Translating cell biology into therapeutic advances in Alzheimer's disease

Article Abstract:

It has been possible to determine the composition of the classical brain lesions in Alzheimer's disease and to identify at least four genes that make people vulnerable to this condition. This has boosted understanding of the genotype-to-phenotype relationships at the heart of inherited types of Alzheimer's disease. It is probable that, in the future, people reaching their 50s or older will be able to have a specific risk-assessment profile to establish their risk of developing Alzheimer's disease.

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