Preventing Cognitive Decline - A Case For Curcumin
The incidence of neurodegenerative diseases in the Asian subcontinent is much lower than in North America. In India, only 0.7% of people aged 70-79 are affected by Alzheimer’s Disease (AD). In contrast, the prevalence in America is more than quadrupled at 3.1%. The reasons for this are hard to elucidate as there are many different environmental and genetic factors, both known and unknown, which make a person more or less prone to developing Alzheimer’s.
One differential aspect between Western and Eastern societies, which may explain this large difference in Alzheimer’s susceptibility, is diet. Oxidative and inflammatory damage has long been associated with Mild Cognitive Impairment (a precursor to Alzheimer’s) and Alzheimer’s disease. It therefore follows that anti-oxidative and anti-inflammatory substances could help protect against neurodegeneration. This has been shown to be the case.
A particular compound, curcumin, has received increasing experimental and clinical attention for it’s potential therapeutic effects. Curcumin is the major active compound present in Turmeric, which is indigenous to the tropical Indian subcontinent. Turmeric is used in a large variety of foods throughout Southern Asia and the Middle East. It is the primary component in yellow curry.
Alzheimer’s disease involves a central nervous system inflammatory response, and AD risk is reduced in those taking non-steroidal anti-inflammatory drugs (NSAID). Novel anti-inflammatory and anti-oxidative compounds are continually researched as possible therapeutic strategies. What makes curcumin special is that it is not only a potent anti-oxidant and anti-inflammatory agent, but it also interacts with and inhibits the aggregation of beta-amyloid fibrils. Oxidative damage is inherent and possibly causal to many age related neurodegenerative diseases, and beta-amyloid plaques are a hallmark of Alzheimer’s pathology.
An in vitro study using fluorescence spectroscopy examined the effects of curcumin on the formation, extension, and destabilization of beta-amyloid fibrils (fAβ). It was found that at physiological pH and temperature, curcumin (Cur) inhibited all three.
“It thus may be reasonable to speculate that Cur could prevent the development of AD not only through scavenging reactive oxygen species but also through directly inhibiting fAβ deposition in the brain.”1
Another study, conducted at the Departments of Medicine and Neurology at UCLA, analyzed the effect of a curcumin diet on memory deficits caused by infusion of amyloid-beta fragments. This is an induced form of memory impairment often used in research. Memory was assessed using a Morris Water Maze (MWM). A MWM is used to track how long it takes a rat to find a hidden platform just below the surface in a container of water. The animals have previously learned the location of the platform, and therefore their ability to remember the location - spatial memory - is assessed. By day three following amyloid-beta infusion, the rats showed spatial memory decline. These rats were then either fed curcumin, or kept on the control diet.
“Compared to Aβ-infused rats fed the control diet, those which were fed curcumin (500 ppm) showed reduced path length and latency in finding the hidden platform, restoring performance to the levels found in the vehicle-infused controls.”2 (The vehicle-infused controls received the same surgery as the experimental group, but were not given Aβ infusion.)
Together, these studies show that curcumin not only inhibits and destabilizes amyloid-beta plaque formation, but also restores memory deficits caused by the presence of these plaques. With these types of results along with the long history of safe curcumin consumption, clinical trials on its effectiveness in AD treatment and prevention were not far off. Paradoxically, clinical trials thus far have been ambiguous. This may be attributable to the small sample size, experimental length of the trials completed so far, and the actual bioavailability of curcumin in the trials.
If you decide you’d like to add curcumin as part of your every day diet, there are a number of ways to go about it. You can take the most natural approach and use ground turmeric and/or yellow curry in your cooking. Curcumin constitutes about 3 percent of turmeric by weight, but can be as high as 5-10%. This may seem like a miniscule amount, but it is still physiologically relevant especially given that the other compounds in turmeric increase the bioavailability of curcumin as compared to taking curcumin alone. However, even though it’s delicious, you may not want to eat curry every day :D
Bioavailability is crucial. Consuming curcumin doesn’t necessarily mean that it’s getting to your brain in a significant amount. Depending on circumstances, some variable portion will be glucuronidated or sulfated by the digestive tract and liver. This “tagged” curcumin will not pass through the blood-brain barrier and therefore will not give us the protective benefits we’re seeking. (Tagged curcumin is also more rapidly cleared by the kidneys.)
Consuming curcumin with fats seems to increase bioavailability, which is typically the case when it’s part of a meal. An alkaloid called piperine, found in black and long pepper, also increases bioavailability through the inhibition of liver glucuronidation. So, if you’d like to take a curcumin supplement, take one encapsulated in a lipid layer or one with added piperine. Pay attention to “free curcumin bioavailability” as opposed to “absorption” or “curcumin bioavailability” as this can include the tagged forms. Paradoxically, if taking a curcumin pill, taking it 3 or more hours after a meal apparently increases bioavailability.
However you decide to consume, curcumin is a great dietary addition to anyone who wishes to lower their chances of cognitive decline with age.
1. Kenjiro Ono1, Kazuhiro Hasegawa, Hironobu Naiki, Masahito Yamada1. Curcumin has potent anti-amyloidogenic effects for Alzheimer's β-amyloid fibrils in vitro. Journal of Neuroscience Research. Volume 75, Issue 6, pages 742–750, 15 March 2004.
2. S.A. Frautschy, W. Hu, P. Kim, S.A. Miller, T. Chu, M.E. Harris-White, G.M. Cole. Phenolic anti-inflammatory antioxidant reversal of Aβ-induced cognitive deficits and neuropathology. Neurobiology of Aging, Volume 22, Issue 6, November–December 2001, Pages 993–1005. http://dx.doi.org/10.1016/S0197-4580(01)00300-1
3. Easton, Mary S. Curcumin. http://alzheimer.neurology.ucla.edu/Curcumin.html
4. Photo Credit: Will Power on Flickr under Attribution 2.0 Generic (CC BY 2.0) License.