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Amyloid /3 peptide, effects

Lambert, L., Mann, D., Goumidi, L., et al. (2001) Effects of the APOE promoter polymorphisms on cerebral amyloid peptide deposition in Alzheimer s disease. Lancet, 357,608-609. [Pg.350]

Takenouchi, T., and Munekata, E. (1994). Inhibitory effects of beta-amyloid peptides on nicotine-induced Ca2+ influx in PC12h cells in culture. Neurosci Lett 773, 147-150. [Pg.522]

In subsequent investigations by Schostarez (4), diaminediol derivatives, (III), effective as (3-secretase enzyme inhibitors were prepared, which were effective in reducing amyloid peptide formation and used in treating dementia and neurodegenerative disorders. [Pg.48]

Muller W.E., Kirsch C., Eckert G.P. Membrane-disordering effects of beta-amyloid peptides. Biochem. Soc. Trans 2001, 29 617-623. [Pg.17]

Kawas CH (2003) Clinical practice. Early Alzheimer s disease. N Engl J Med 349 1056-1063 Kaye JA (1998) Diagnostic challenges in dementia. Neurology 51 S45-S52 discussion S65-47 Keller JN, Lauderback CM, Butterfield DA, Kindy MS, Yu J, Markesbery WR (2000) Amyloid beta-peptide effects on synaptosomes from apolipoprotein E-deficient mice. J Neurochem 74 1579-1586... [Pg.741]

In addition, vaccination against the suspected culprit of the disease, th< -amyloid peptide, which aggEgates into the plaques and which is formed by - and -secretases, is being tested. The first vaccination studies against -amyloid peptide wear effective in Emoving some of the peptide fom the brain in humans and in experimental animals—evenducing the number of plaques. But these studies have been stopped because of safety issues. [Pg.271]

Shen C-L, Murphy RM. Solvent effects on self-assembly of P-amyloid peptide. Biophys. J. 1995 69 640-651. [Pg.1946]

Congo red (C.l. Direct red 28 direct red C.l. 22120) is an azo dye, often used as the disodium salt. It inhibits neurotoxic effects of fibrillar p-amyloid peptides (implications for treatment of Alzheimer s disease). It also inhibits replication and accumulation of the agent responsible for scrapie. It is an indicator used as a diagnostic agent for amyloidosis. It is also used to detect acute-phase serum proteins. [Pg.83]

Qin L, Zhang J, Qin M (2013) Protective effect of cyanidin 3-O-glucoside on beta-amyloid peptide-induced cognitive impairment in rats. Neurosci Lett 534 285-288... [Pg.534]

Mattson, M. R, Tomaselli, K. J., and Rydel, R.E., Calcium-destabilizing and neuro-degenerative effects of aggregated beta-amyloid peptide are attenuated by basic FGF, Brain Res., 621, 35, 1993. [Pg.210]

Thioflavin T (ThT) fluorescence measurements (Jarrett and Lansbury, 1993) enabled us to reveal that BChE is capable of attenuating the in vitro formation of amyloid fibrils from the AD beta-amyloid peptide, unlike AChE-S, which facilitates such fibril formation. The C-terminal of BChE was identified as responsible for this attenuation function, and a synthetic peptide having the C-terminal sequence of human BChE, BSP41 was found capable of performing a similarly effective attenuation of fibril formation as BChE. AChE-S, in comparison, promoted fibril formation, and its C-terminal peptide, ASP40, failed to affect this process. [Pg.204]


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