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Alzheimer's Disease Functional Foods

Cinnamon Compound May Prevent Alzheimer’s

6 years, 12 months ago

1884  0
Posted on Jul 21, 2011, 6 a.m.

Israeli team finds that CEppt, an extract found in cinnamon bark, exhibits properties that can inhibit the development of Alzheimer’s Disease.

With an estimated one in eight Americans over the age of 65 afflicted with Alzheimer’s Disease, and a continuance in gains that extend the length of the average lifespan, the disease is projected to exert a major societal and economic burden in the coming years.  Michael Ovadia, from Tel Aviv University (Israel), and colleagues isolated CEppt, an extract found in cinnamon bark, and introduced the substance into the drinking water of mice that had been genetically altered to develop an aggressive form of Alzheimer's disease, and fruit flies that had been mutated with a human gene that also stimulated Alzheimer's disease and shortened their lifespan. After four months, the researchers discovered that development of the disease had slowed remarkably and the animals' activity levels and longevity were comparable to that of their healthy counterparts. The extract inhibited the formation of toxic amyloid polypeptide oligomers and fibrils, which compose deposits of plaque found in the brains of Alzheimer's patients.  In a test-tube study, CEppt was also found to break up amyloid fibers, similar to those seen in Alzheimer's patients.  Noting that CEppt caused a “reduction of plaques and improvement in cognitive behavior,” the team concludes that:  “Our results present a novel prophylactic approach for inhibition of toxic oligomeric A[beta] species formation in [Alzheimer’s Disease] through the utilization of a compound that is currently in use in human diet.”

Frydman-Marom A, Levin A, Farfara D, Benromano T, Scherzer-Attali R, Peled S, Vassar R, Segal D, Gazit E, Frenkel D, Ovadia M. “Orally administrated cinnamon extract reduces [beta]-amyloid oligomerization and corrects cognitive impairment in Alzheimer's disease animal models.” PLoS One. 2011 Jan 28;6(1):e16564.

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