Een zekere Dr. K. suggereerde dat het mogelijk door de genen kwam dat een bepaalde bevolkingsgroep niet of nauwelijks ontvankelijk was voor Alzheimer. Maar onderzoeken van diverse Universiteiten, zoals de onderstaande, laten zien dat curcumin in werkelijkheid de werkzame stof is; GRECC (VA Medical) and Medicine, University of California Los Angeles, North Hills, CA 91343 Corresponding Author: firstname.lastname@example.org
Alzheimer’s disease (AD) involves amyloid (A ) accumulation, oxidative damage and inflammation, and risk is reduced with increased antioxidant and anti-inflammatory consumption. The phenolic yellow curry pigment curcumin has potent anti-inflammatory and antioxidant activities and can suppress oxidative damage, inflammation, cognitive deficits, and amyloid accumulation. Since the molecular structure of curcumin suggested potential Aß-binding, we investigated whether its efficacy in AD models could be explained by effects on Aß aggregation. Under aggregating conditions in vitro, curcumin inhibited aggregation (IC50 =0.8 µM) as well as disaggregated fibrillar Aß40 (IC50 =1 µM), indicating favorable stoichiometry for inhibition. Curcumin was a better A 40 aggregation inhibitor than ibuprofen and naproxen, and prevented A 42 oligomer formation and toxicity between 0.1-1.0 M. Under electron microscopy, curcumin decreased dose-dependently Aß fibril formation beginning with 0.125 µM. Curcumin’s effects did not depend on A sequence but on fibril-related conformation. AD and Tg2576 mice brain sections incubated with curcumin revealed preferential labelling of amyloid plaques. In vivo studies showed that curcumin injected peripherally into aged Tg mice, crossed the blood brain barrier and bound plaques. When fed to aged Tg2576 mice with advanced amyloid accumulation, curcumin labeled plaques and reduced amyloid levels and plaque burden. Hence, curcumin directly binds small ß-amyloid species to block aggregation and fibril formation in vitro and in vivo. These data suggest that low dose curcumin effectively disaggregates Aß as well as prevents fibril and oligomer formation, supporting the rationale for curcumin use in clinical trials preventing or treating AD.
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