11.26.2004

New Treatment Target for Alzheimer's
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Scientists have identified a new, longer species of amyloid beta-peptide that has the potential to be a new target for the treatment of Alzheimer's disease, according to research published in the Journal of Biological Chemistry, an American Society for Biochemistry and Molecular Biology journal.

Scientists have identified a new, longer species of amyloid beta-peptide that has the potential to be a new target for the treatment of Alzheimer's disease, according to research published in the Journal of Biological Chemistry, an American Society for Biochemistry and Molecular Biology journal.

One of the characteristic features of Alzheimer's disease is the deposition of amyloid beta-peptides in the brain. These amyloid beta-peptides are derived from a large amyloid precursor protein through a series of cleavage events.

Under normal conditions, cleavage first by alpha-secretase and then by gamma-secretase results in a soluble ectodomain, a short peptide called p3, and an intracellular C-terminal domain, none of which are amyloidogenic.

Alternatively, amyloid precursor protein can be processed by the enzymes beta-secretase and gamma-secretase to produce a soluble ectodomain along with the full-length amyloidogenic amyloid beta-peptide and the intracellular C-terminal domain.

Although amyloid precursor protein is found in many cells, its normal biological function is not well understood.

While the exact pathogenic role of amyloid beta-peptide in Alzheimer's disease has not yet been definitely established, accumulating evidence supports the hypothesis that amyloid beta-peptide production and deposition in the brain could be a causative event in Alzheimer's disease.

Dr Xuemin Xu of the University of Tennessee explains that the literature indicates amyloid beta-peptide itself could be toxic to synapses and the accumulation of amyloid beta-peptide could initiate a series of events contributing to cell death, including activation of cell death programs, oxidation of lipids and disruption of cell membranes, an inflammatory response, and possibly neurofibrillary tangle formation, which is a close correlate



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