Turmeric Curry May Keep Alzheimer's at Bay
A spice used for thousands of years, curry, may be a powerful new weapon in fighting Alzheimer's Disease, researchers said.
Researchers from UCLA and the Department of Veterans Affairs said their study of curcumin, the yellow pigment in curry, found it broke up existing beta amyloid on rats' brains and helped prevent accumulation of the destructive plaque.
Reporting in the Journal of Biological Chemistry, the team said curcumin is more effective in stopping the protein fragments from forming than many other drugs being tested to treat the disease that affects 4 million Americans and millions more worldwide. "The prospect of finding a safe and effective new approach to both prevention and treatment of Alzheimer's disease is tremendously exciting," said Gregory Cole, the main UCLA investigator.
"Curcumin has been used for thousands of years as a safe anti-inflammatory in a variety of ailments as part of Indian traditional medicine," Cole said. Recent animal studies "support a growing interest in its possible use for diseases of aging involving oxidative damage and inflammation like Alzheimer's, cancer and heart disease."
Cole called for human trials of curcumin to establish safe and effective doses.
Curcumin inhibits formation of Abeta oligomers and fibrils and binds plaques and reduces amyloid in vivo
By GRECC (VA Medical) and Medicine, University of California Los Angeles
Alzheimer's disease involves amyloid (Abeta) 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 Alzheimer's disease models could be explained by effects on Ass aggregation. Under aggregating conditions in vitro, curcumin inhibited aggregation (IC(50) =0.8 microM) as well as disaggregated fibrillar Ass40 (IC(50) =1 microM), indicating favorable stoichiometry for inhibition. Curcumin was a better Abeta40 aggregation inhibitor than ibuprofen and naproxen, and prevented Abeta42 oligomer formation and toxicity between 0.1-1.0 muM. Under electron microscopy, curcumin decreased dose-dependently Ass fibril formation beginning with 0.125 microM. Curcumin's effects did not depend on Abeta sequence but on fibril-related conformation. Alzheimer'sdisease and Tg2576 mice brain sections incubated with curcumin revealed preferential labeling 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 Alzheimer's disease.
Yang F, Lim GP, Begum AN, Ubeda OJ, Simmons MR, Ambegaokar SS, Chen PP, Kayed R, Glabe CG, Frautschy SA, Cole GM.
GRECC (VA Medical) and Medicine, University of California Los Angeles, North Hills, CA 91343.
Curcumin, the activeconstituent of turmeric, inhibits amyloid peptide-induced cytochemokinegene expression and CCR5-mediated chemotaxis of THP-1 monocytes by modulating early growth response-1 transcription factor.
Epidemiological studies show reduced risk of Alzheimer's disease among patients usingnon-steroidal inflammatory drugs (NSAID) indicating the role of inflammation in Alzheimer's disease. Studies have shown a chronic CNS inflammatory response associated with increased accumulation of amyloid peptide and activated microglia in Alzheimer's disease. Our previous studies showed that interaction of Abeta1-40 or fibrilar Abeta1-42 caused activation of nuclear transcription factor, early growth response-1 (Egr-1), which resulted in increased expression of cytokines (TNF-alpha and IL-1beta) and chemokines (MIP-1beta, MCP-1 and IL-8) in monocytes. We determined whether curcumin, a natural product known to have anti-inflammatory properties, suppressed Egr-1 activation and concomitant expression of cytochemokines. We show that curcumin (12.5-25 microm) suppresses the activation of Egr-1 DNA-binding activity in THP-1 monocytic cells. Curcuminabrogated Abeta1-40-induced expression of cytokines (TNF-alpha and IL-1beta)and chemokines (MIP-1beta, MCP-1 and IL-8) in both peripheral blood monocytesand THP-1 cells. We found that curcumin inhibited Abeta1-40-induced MAPkinase activation and the phosphorylation of ERK-1/2 and its downstream target Elk-1. We observed that curcumin inhibited Abeta1-40-induced expressionof CCR5 but not of CCR2b in THP-1 cells. This involved abrogation of Egr-1DNA binding in the promoter of CCR5 by curcumin as determined by: (i) electrophoretic mobility shift assay, (ii) transfection studies with truncated CCR5 gene promoter constructs, and (iii) chromatin immunoprecipitation analysis. Finally, curcumin inhibited chemotaxis of THP-1 monocytes inresponse to chemoattractant. The inhibition of Egr-1 by curcumin may represent a potential therapeutic approach to ameliorate the inflammation and progression of Alzheimer's disease.
Giri RK, Rajagopal V, Kalra VK.
Department of Biochemistry and Molecular Biology, University of Southern California, Keck School of Medicine, Los Angeles, California 90033, USA.
Alzheimer's Research
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