In India, the prevalence of Alzheimer's disease among 70- to 79-year-olds is 4.4-fold less than that of the United States. Could they have one of the curry spices to thank for that? So suggest Greg Cole, Giselle Lim, and colleagues at the University of California and the Los Angeles Veterans Affairs Administration in an article in today's Journal of Neuroscience.

Since it became clear that AD is characterized by chronic inflammation and oxidative damage-and that patients taking nonsteroidal antiinflammatory drugs (NSAIDs) had a reduced risk of AD-researchers have focused attention on strategies to reduce these interrelated cytotoxic processes in AD. There has been a particular interest in finding alternatives to NSAIDs, which have significant side effects with long-term use.

Cole and his colleagues noted that curcumin, a yellow curry spice derived from turmeric, is a potent antioxidant. It is several times more potent a free radical scavenger than vitamin E (α-tocopherol), which has been unsuccessfully tested as a therapy to slow the progression of AD. The researchers tested two dietary doses (160 and 5,000 ppm) of curcumin on APPSw transgenic mice. Thanks to the defective AβPP gene from a Swedish family with hereditary AD, these mice display some of the hallmarks of AD (the accumulation of neuritic plaques, memory deficits as they age, as well as chronic inflammatory responses and oxidative damage). After being fed curcumin from the age of 10 to 16 months, mice in both the low- and high-dose groups had significantly lower brain levels of oxidized proteins and interleukin-1, a proinflammatory cytokine. With the lower dose only, there were significant reductions in the astrocytic marker GFAP (associated with injury and inflammatory processes), and in insoluble Aβ, soluble Aβ, and plaque burden.

"In light of its efficacy and apparent low toxicity, this Indian spice component shows promise for the prevention Alzheimer's disease," conclude the authors.—Hakon Heimer


  1. I liked the paper very much. It is generally well done and suggests an easy intervention that could reduce AD onset or progression without significant toxicity. Among the questions it raises are:

    1.) How does the concentration of curcumin that is effective in the APPSw mice compare to that normally ingested in countries where curcumin is a staple?

    2.) Can curcumin be given after the pathology has started, or does it need to be taken for a long time prior to symptoms?

    3.) It would be helpful to compare the effects of curcumin on inflammatory oxidative markers in the APPSw mice with the effects of giving vitamin E, vitamin E and NSAIDs, as the authors argue that curcumin is more beneficial because it combines the properties of an antioxidant and NSAID.

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Primary Papers

  1. . The curry spice curcumin reduces oxidative damage and amyloid pathology in an Alzheimer transgenic mouse. J Neurosci. 2001 Nov 1;21(21):8370-7. PubMed.