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By Takaomi Comings Saido

Beta-secretase M. Citron Alpha-secretases S. Ishiura ADAM 10/alpha secretase and presenilins/gamma secretase in APP processing and notch signaling D. Hartmann Gamma-secretase and presenilin M. Wolfe Biochemistry of gamma-secretase (tentative name) S. Sinha Presenilin and intracellular protein delivery Degradation of Abeta through neprilysin T.C. Saido Degradation of Abeta via endothelin-converting enzyme C. Eckman Degradation of Abeta by way of insulin-degrading enzyme Lipid raft and Abeta metabolism T. Golde Lipid raft and Abeta accumulation M. Morishima-Kawashima and Y. Ihara Transport-dependent clearance of Abeta B. Zlokovic Abeta vaccination C. Lemere

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Extra resources for A-Beta Metabolism and Alzheimer's Disease (Neuroscience Intelligence Unit 7)

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Stars represent sites of missense mutation that cause familial Alzheimer’s disease. The two conserved aspartates required for presenilin endoproteolysis and γ-secretase processing of APP and Notch are predicted to be within TM6 and TM7. The region of the protein encoded by exon 9 is denoted; natural deletion of this exon leads to a noncleavable but functional presenilin. 36,37 Unfortunately, the embryonic lethality resulting from deleting PS1 did not suggest reasons why PS mutations might cause AD relatively late in life.

Amyloid: Int J Exp Clin Invest 1994; 1:263-280. 7. Vassar R, Bennett BD, Babu-Khan S et al. β-secretase cleavage of Alzheimer’s amyloid precursor protein by the transmembrane aspartic protease BACE. Science 1999; 286:735-741. 8. Yan R, Bienkowski MJ, Shuck ME et al. Membrane-anchored aspartyl protease with Alzheimer’s disease β-secretase specificity. Nature 1999; 402:533-537. 9. Sinha S, Anderson JP, Barbour R et al. Purification and cloning of amyloid precursor protein β-secretase from human brain.

The results indicate that ADAM9, ADAM10 and ADAM17 catalyze α-secretory cleavage and therefore act as α-secretases in A172 cells. Despite our lack of full knowledge concerning the identity of APP α-secretase, it is clear that the activation of these proteases may offer new therapeutic methods. Inhibitors of β- and γ-secretases may prevent the deposition of Aβ in brain, whereas an activator of α-secretase (and Aβ-degrading enzymes) may inhibit the accumulation of Aβ with the same efficiency. There is strong evidence to suggest that NSAIDs may prevent or delay the onset of Alzheimer’s disease.

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