Curcumin, the Curry Spice
Part 4

A look at how curcumin affects cells in Alzheimer’s disease and how this research may relate to HD

Uncertainties in How the Animal Research Relates to Humans

The AD mice study mentioned in the above sections prompts us to offer some cautionary notes about directly applying results from mice to humans:

First, the AD study tested curcumin by splitting the mice into three groups: one group received a low dose of curcumin, another group received a high dose, and the third group received no curcumin at all. Curiously, comparing the low-dose group and high-dose group, low doses of curcumin actually appeared to combat neurodegeneration in AD better than high doses. While the reason for this finding is not yet fully understood, the results do tell us something important: just because a substance is helpful does not mean its helpfulness is increased with every increase in dosage. In fact, increased or prolonged dosages of an initially helpful substance can actually be harmful. In the ibuprofen study mentioned above, for example, gastrointestinal, liver, and kidney damage resulted from the prolonged use of otherwise helpful ibuprofen.

Second, it is also important to keep in mind that mice, of course, have significantly smaller bodies than humans and may metabolize substances differently than we do. Thus, despite its apparent safety in animal studies (for example, one study on mice used 83 times the normal amount of curcumin, and still produced no mortalities), one should always exercise caution when using a new substance (medicinal or natural) to treat a disorder. And as always, for advice about treating disease, it is important to consult a physician.

Clinical trials should soon be underway in order to establish the safety of using curcumin to combat AD in humans. If future laboratory and animal studies suggest that curcumin holds promise for combating Huntington's disease as well, then clinical trials to test its safety and effectiveness in HD would also be needed.

We hope you enjoyed this section of the HOPES website. To email this article to a friend, please click here. To leave feedback for the HOPES team, click here. Make sure to specify which article you're referring to.

-M. Stenerson, 6-28-04

For further reading:

1. Heiser V, Scherzinger E, Boeddrich A, Nordhoff E, Lurz R, Schugardt N, Lehrach H, Wanker EE. Inhibition of huntingtin fibrillogenesis by specific antibodies and small molecules: implications for Huntington's disease therapy. Proc Natl Acad Sci U S A. 2000 Jun 6;97(12):6739-44. PMID: 10829068 [PubMed - indexed for MEDLINE]
   A technical paper that describes the effectiveness of certain compounds in decreasing the amount of huntingtin protein aggregation in HD.
2. Lim GP, Chu T, Yang F, Beech W, Frautschy SA, Cole GM. The curry spice curcumin reduces oxidative damage and amyloid pathology in an Alzheimer transgenic mouse. . J Neurosci. 2001 Nov 1;21(21):8370-7. PMID: 11606625 [PubMed - indexed for MEDLINE]
   A technical paper that discusses how curcumin affects the nerve cells of Alzheimer's mice. This is the paper on which the majority of the chapter was based.
3. Scherzinger E, Sittler A, Schweiger K, Heiser V, Lurz R, Hasenbank R, Bates GP, Lehrach H, Wanker EE. Self-assembly of polyglutamine-containing huntingtin fragments into amyloid-like fibrils: implications for Huntington's disease pathology. Proc Natl Acad Sci U S A. 1999 Apr 13;96(8):4604-9. PMID: 10200309 [PubMed - indexed for MEDLINE]
   A technical paper that discusses the similarities between huntingtin protein aggregates and beta-amyloid fibrils.

Last Modified: 6-28-04

An educational product of HOPES, not to be used in place of medical care. For more information about HOPES, click on the Logo. To contact HOPES with comments or questions, click here.