Curcumin, the Curry Spice
Part 3

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

How this Alzheimer's Research May Affect Huntington's Disease

Although research to confirm such a notion is just now getting underway, the results of the Alzheimer's study suggest that curcumin might well be helpful in combating other neurodegenerative diseases like HD. Despite the differences in the fundamental "cause" of each disease - HD is believed to be a purely genetic disorder, while AD is believed to have both genetic and environmental components - the damage to nerve cells in each disorder is strikingly similar. Thus, because curcumin combats the phenomena that contribute to neurodegeneration in AD, it is fair to suggest that the substance may possibly be capable of combating similar phenomena in HD.

Just as in Alzheimer's, inflammation and oxidative damage play a strong role in the neurodegenerative process of HD: oxidative damage (also known as "oxidative stress") helps to degrade nerve cells in the basal ganglia and cerebral cortex; chronic inflammation in the brains of people with HD is believed to play a significant role in the progression of the disease. ( For more info about inflammation, click here.) As shown previously, curcumin was able to reduce inflammation and oxidative damage in mouse models of AD. Although it is possible that the pattern of inflammation in the brain and the severity of oxidative damage may be different between AD and HD, if they are even slightly similar in the two disorders, then one would expect curcumin to also have a positive effect on combating HD.

Despite the harmful effects of inflammation and oxidative damage, beta-amyloid fibrils (which make up beta-amyloid plaques) have won the most attention among researchers and the general public with regard to AD. Similarly, despite the harmful effects of other phenomena that contribute to neurodegeneration, the most attention among researchers and the general public with regard to Huntington's disease is devoted to huntingtin protein aggregation. The attention paid to beta-amyloid fibrils and huntingtin protein aggregation is not unjustified: in addition to being telltale signs of their respective disorders, these two phenomena may be key players in the neurodegenerative process. For instance, some researchers believe that substances which inhibit huntingtin protein aggregation will also be found to inhibit the initial structural alteration of the huntingtin protein, an alteration that is believed to start the entire disease process in HD. But there is another discovery that could have potentially profound effects on the research underway for both of these diseases: based on their ribbon-like structure and the mechanism by which they are created, huntingtin protein aggregates are quite similar to beta-amyloid fibrils. Given this discovery, it is possible that substances that decrease the presence of beta-amyloid fibrils may do the same with huntingtin protein aggregates, and vice-versa.

As of this writing (June 2004), research on the effectiveness of curcumin in combating huntingtin protein aggregation has just gotten underway. Should curcumin prove to decrease huntingtin protein aggregates as well as it did beta-amyloid plaques, this would be a true triumph in HD research. However, while this possibility is certainly a source of intrigue, it is important to note that not all substances that are proven to decrease beta-amyloid levels have shown the same effectiveness with huntingtin protein aggregation. For instance, the compounds thioflavine T, gossypol, melatonin, and rifampicin, all of which are believed to decrease the presence of beta-amyloid, had little or no success in inhibiting huntingtin protein aggregation. On the other hand, Congo Red and thioflavine S, which are also believed to decrease beta-amyloid, did effectively decrease huntingtin protein aggregation. Thus, while the similarities between beta-amyloid fibrils and huntingtin protein aggregates make us hopeful that curcumin can decrease the aggregates, current research on curcumin and HD will have the final say.

A closing remark: This section lacks definitive answers about how curcumin affects HD for one reason: the research simply has not yet been done. As the studies that are currently underway produce results, and as potentially more studies are begun, we will learn a great deal about how curcumin affects HD.

Last Modified: 7-6-04

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