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More on Curcumin and Alzheimer's Treatment & Prevention

This is an interesting study that looked at the plaques, themselves in Alzheimer's Disease.  Studies, such as this one, are used to develope pharmaceutical 'improvements' to naturally occurring compounds.  By altering the non-patentable, naturally occuring compounds, companies can introduce patented pharmaceuticals.  While this is often beneficial to the consumer, just as often it is a more expensive alternative to the naturally occuring substances.

 

Case in point:  "Gee, I remember when fish oil was ineffective to treat anything, let alone heart disease."  Now that there is a prescription fish oil product, it magically works.  Go figure.

 

Ono K, Naiki H, & Yamada M:   The development of preventives and therapeutics for Alzheimer's disease that inhibit the formation of beta-amyloid fibrils (fAbeta), as well as destabilize preformed fAbeta.Curr Pharm Des:   2006;12(33):4357-75.

Neuritic plaques composed mainly of amyloid beta-protein (Abeta) in the brain are an early and invariant neuropathological feature of Alzheimer's disease (AD). The current search for anti-AD drugs is mainly focused on modification of the process of Abeta deposition in the brain. In this article, the recent development of the molecules that inhibit the formation of beta-amyloid fibrils (fAbeta), as well as destabilize preformed fAbeta is reviewed. Recently, various compounds such as curcumin, nicotine and wine-related polyphenols have been reported to inhibit the formation, extension of fAbeta, as well as destabilize preformed fAbeta at pH 7.5 at 37 degrees C in vitro. In cell culture experiments, destabilized fAbeta were suggested to be less toxic than intact fAbeta. In transgenic mice model study, some coumpounds such as curcumin and nicotine have also been reported to reduce plaque burden in vivo. Although the mechanisms by which these compounds inhibit fAbeta formation from Abeta, and destabilize preformed fAbeta are still unclear, they could be key molecules for the development of preventives and therapeutics for AD.

Note: 

Even the highest quality, pharmaceutical grade Curcumin is inexpensive.  For Alzheimer's Disease, recommend 500-600 mg of curcumin, once or twice daily. For Alzheimer's Prevention, 500-600 mg once daily is probably enough. 

I use the Silymarin/curcumin combination in men, three times daily, but it can lower estrogen levels in women, so it needs to be used in females more carefully.

 

 

Curcumin as a treatment/preventative agent for Alzheimer's Disease

NOTE: 

1. While technical in nature, this study demonstrates the value of Curcumin in the treatment of Alzheimer's Disease, and demonstrates the biochemical basis of action. 
2. Why wait for the medical community to recommend this inexpensive, available and safe nutraceutical if there is a reasonable expectatation that it may treat, prevent or forstall the development of Alzheimer's Disease?

Begum AN, Jones MR, Lim GP, et al: Curcumin structure-function, bioavailability, and efficacy in models of neuroinflammation and Alzheimer's disease. J Pharmacol Exp Ther: 2008 Jul;326(1):196-208. 

Curcumin can reduce inflammation and neurodegeneration, but its chemical instability and metabolism raise concerns, including whether the more stable metabolite tetrahydrocurcumin (TC) may mediate efficacy. We examined the antioxidant, anti-inflammatory, or anti-amyloidogenic effects of dietary curcumin and TC, either administered chronically to aged Tg2576 APPsw mice or acutely to lipopolysaccharide (LPS)-injected wild-type mice. Despite dramatically higher drug plasma levels after TC compared with curcumin gavage, resulting brain levels of parent compounds were similar, correlating with reduction in LPS-stimulated inducible nitric-oxide synthase, nitrotyrosine, F2 isoprostanes, and carbonyls. In both the acute (LPS) and chronic inflammation (Tg2576), TC and curcumin similarly reduced interleukin-1beta. Despite these similarities, only curcumin was effective in reducing amyloid plaque burden, insoluble beta-amyloid peptide (Abeta), and carbonyls. TC had no impact on plaques or insoluble Abeta, but both reduced Tris-buffered saline-soluble Abeta and phospho-c-Jun NH(2)-terminal kinase (JNK). Curcumin but not TC prevented Abeta aggregation. The TC metabolite was detected in brain and plasma from mice chronically fed the parent compound. These data indicate that the dienone bridge present in curcumin, but not in TC, is necessary to reduce plaque deposition and protein oxidation in an Alzheimer's model. Nevertheless, TC did reduce neuroinflammation and soluble Abeta, effects that may be attributable to limiting JNK-mediated transcription. Because of its favorable safety profile and the involvement of misfolded proteins, oxidative damage, and inflammation in multiple chronic degenerative diseases, these data relating curcumin dosing to the blood and tissue levels required for efficacy should help translation efforts from multiple successful preclinical models.

For more information:  www.suffernomore.com

note:

Even the highest quality, pharmaceutical grade Curcumin is inexpensive.  For Alzheimer's Disease, recommend 500-600 mg of curcumin, once or twice daily. For Alzheimer's Prevention, 500-600 mg once daily is probably enough. 

I use the Silymarin/curcumin combination in men, three times daily, but it can lower estrogen levels in women, so it needs to be used in females more carefully.