• Biochem. Biophys. Res. Commun. · Dec 2002

    alpha- and beta-secretase: profound changes in Alzheimer's disease.

    • Susan J Tyler, David Dawbarn, Gordon K Wilcock, and Shelley J Allen.
    • Molecular Neurobiology Unit, URCN (Care of the Elderly) University of Bristol, Bristol Royal Infirmary, Bristol, UK.
    • Biochem. Biophys. Res. Commun. 2002 Dec 6; 299 (3): 373-6.

    AbstractThe amyloid plaque, a neuropathological hallmark of Alzheimer's disease, is produced by the deposition of beta-amyloid (Abeta) peptide, which is cleaved from Amyloid Precursor Protein (APP) by the enzyme beta-secretase. Only small amounts of Abeta form in normal brain; more typically this is precluded by the processing of APP by alpha-secretase. Here, we describe a decrease in alpha-secretase (81% of normal) and a large increase in beta-secretase activity (185%) in sporadic Alzheimer's disease temporal cortex. Since alpha-secretase is present principally in neurons known to be vulnerable in Alzheimer's disease, and there is known competition between alpha- and beta-secretase for the substrate APP, it is significant that the majority of Alzheimer samples tested here were low in alpha-secretase. Eighty percent of Alzheimer brains examined had an increase in beta-secretase, a decrease in alpha-secretase, or both; which may account for the means by which the majority of people develop Alzheimer's disease.

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