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Alzheimer’s disease creates an accumulation of amyloid plaque deposits, which is composed primarily of the neurotoxic beta-amyloid peptide. The amyloid peptides are “cut” out from a larger protein called amyloid precursor protein (APP), then bind together to form plaques in the memory area of the brain.

Vivian Y.H. Hook, PhD, professor, Skaggs School of Pharmacy and Pharmaceutical Sciences, University of California at San Diego, has discovered 2 chemical compounds that inhibit a new enzyme target that reduces the production of beta-amyloid, which improved the memories in mice genetically engineered with the Alzheimer’s disease gene.

Previously, scientists focused on mutant beta-secretase sequence, which was only seen in one extended family of Swedish patients diagnosed with Alzheimer’s. Research had discovered that this Swedish mutant sequence is cut by a protease called BACE1. Hook, and fellow researchers, found that a different protease called Cathepsin B (CatB) is what cuts the beta-secretase sequence found in 99% of Alzheimer’s patients outside the Swedish family that has been the subject of other studies.

Mice genetically engineered with Alzheimer’s disease exhibited a great improvement in their memory (as well as reduced brain levels of beta amyloid) after they had been given a drug compound¬†that targets Cathepsin B. By disabling the enzyme’s ability to cut the ‘beta’ end of the amino acid sequence, researchers may discover a way to limit production of neurotoxic A? and reduce amyloid plaques in the brain.

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