Plants have a long history as a rich source of new compounds for drug discovery. Cinnamon is widely used by humans, both as a spice and as a traditional medicine. It is, perhaps, one of the oldest herbal medicines, having been mentioned in the Bible and in Chinese texts as long as 4,000 years ago.
Previous studies have already demonstrated the potential for herbal extracts to interact with beta-amyloid, and perhaps slow down or even prevent AD. As we move towards earlier identification of Alzheimer’s disease pathology in minimally symptomatic individuals, such therapies will undoubtedly become areas of intense research. Examples for extensively studied naturally occurring compounds are the (-)-epigallocatechin-3-gallate (EGCG) from green tea and Curcumin, which is derived from the natural turmeric.
Now, a research team headed by Michael Ovadia from Tel Aviv University, has isolated one of the ingredients in cinnamon, CEppt, and used it in a series of tests conducted on two-month-old lab mice that were raised with five aggressive strains of Alzheimer’s-inducing genes. The experiment’s results, recently published in the PLoS ONE scientific journal, were impressive. Laboratory rodents, genetically altered to develop dementia, received either the cinnamon extract or an inert treatment for four months. The extract improved the rats’ performance on learning and memory tasks. It also reduced the amount of plaque formed in the brain. The animals were fed drinking water containing a CEppt solution over four months, and researchers found that the disease’s development was delayed, with additional trials showing that existing amyloids had been dissolved. The results show the ability of CEppt to inhibit the progress of beta-amyloid aggregation. CEppt is actually comprised of several molecules, and it remains to be found which molecule is exerting this effect.
Supplements such as Curcumin, EGCG, DHA and CEppt will likely be evaluated in clinical trials in patients who have minimal symptoms, but are on the path towards developing AD. That is, patients with amyloid building up in the brain, but not yet showing symptoms as assessed by Amyloid scans (for example. From studies such as ADNI, we believe that there is a 15 year window during which amyloid is building up in the brain, while there are minimal symptoms, such as memory loss present. This window may be the best time to initiate anti-amyloid therapy.)
Director, Memory Disorders Clinic
Associate Medical Core Director, Alzheimer’s Disease Cooperative Study
University of California San Diego
This post originally appeared in Alzheimer’s Insights, an ADCS Blog.