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Chris D. Meletis, ND
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- 2011-09-14 16:09:18
2012-04-29 01:23:08 - Harnessing the Power of Ashwaghanda for the brain---It supports more than the adrenals
Withania somnifera Studied for Brain Health and Cognition
Researchers found that Withania somnifera modulates Alzheimer’s disease pathology, according to a study published in February 2012. Withania somnifera (ashwagandha) is a commonly used botanical in Ayurvedic medicine for its rejuvenating and antioxidant properties and modulation of inflammatory pathways, the stress response and immune system activity.
The study used transgenic mice with accelerated Alzheimer’s disease pathology and beta-amyloid plaque deposition, which is implicated in the development of Alzheimer’s disease. The mice received Withania somnifera root extract for 30 days.
Withania somnifera administration resulted in reversal of behavioral deficits, plaque pathology and accumulation of beta-amyloid peptides in the brains of middle-aged and old mice. In addition, after seven days of Withania somnifera administration, beta-amyloid peptides were increased in the plasma and decreased in the brain, indicating increased transport of the peptides from the brain to the periphery.
Also after seven days, there was an increase in low-density lipoprotein receptor-related protein and the beta-amyloid peptide-degrading protease neprilysin in the liver and a rise in plasma soluble low-density lipoprotein receptor-related protein. After 14 to 21 days of declining beta-amyloid peptides in the brain, the researchers found an increase in the expression of low-density lipoprotein receptor-related protein in brain microvessels and neprilysin. The researchers state that this promotes clearance of brain beta-amyloid peptides.
The investigators concluded, "The remarkable therapeutic effect of Withania somnifera mediated through up-regulation of liver low-density lipoprotein receptor-related protein indicates that targeting the periphery offers a unique mechanism for beta-amyloid peptide clearance and reverses the behavioral deficits and pathology seen in Alzheimer's disease models.”
Sehgal N, et al. Proc Natl Acad Sci U S A. 2012;9:3510-5.
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Chris D. Meletis, ND
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