Can Ashwagandha Reverse Alzheimer’s Disease?

Post on March 5, 2015 by André Broussard, D.C.

Maylin Rodriguez Paez RN

Ashwagandha is one of the most popular herbs in Ayurvedic medicine.

Native to Asia, it’s been used for thousands of years for different ailments including insomnia, anxiety, and even sexual dysfunction.

Research shows ashwagandha may also have potential in treating Alzheimer’s disease. It clears amyloid plaque, a key feature of the condition. 

Ashwagandha Reverses Cognitive Deficits

Building on previous work which demonstrated the neuro-regenerative properties of ashwagandha, researchers tested its effect on Alzheimer’s disease.

A group of rats with the condition were administered a placebo or ashwagandha root for 30 days. After 20 days, the mice receiving the ashwagandha started exhibiting improved cognitive function.

They were able to navigate through maze tests from which they had difficulty prior to supplementation. This demonstrated an improvement in spatial memory and learning.1

In addition, they experienced a reduction in amyloid plaque in different parts of the brain including the cortex and the hippocampus, the area in which memories are stored.

Ashwagandha: A Potential Brain Drug?

Current medications for Alzheimer’s disease target symptoms, but fall short of addressing the underlying contributing factors. They do not reverse its progression or provide a cure. Ashwagandha, on the other hand, attacks multiple aspects of the disease.

Human clinical trials are needed, but so far cell culture and animal studies show promising results. Here are some of the findings showing it may have potential as a future Alzheimer’s medication:

  • It restores synapses, the junctions where nerve cells communicate with other cells, after amyloid-induced injury.2 One characteristic of Alzheimer’s disease is decreased synaptic density.
  • It supports the growth of dendrites, the short branched extensions of a nerve cell.2
  • It regenerates axons, the long threadlike part of a nerve which transmits impulses.2
  • It increases neurite growth.2
  • It protects against glutamate, an excitatory neurotransmitter, which destroys brain cells and plays a role in Alzheimer’s disease.3
  • It decreases reaction times in human clinical trials.4
  • It protects brain cells from beta-amyloid-induced cell damage.5
  • It guards brain cells against free radicals that are implicated in Alzheimer’s disease.6
  • It inhibits acetylcholinesterase, the enzyme that breaks down acetylcholine. Current medications used to treat Alzheimer’s disease function via this mechanism.7

References:

  1. Proc Natl Acad Sci U S A. 2012 February 28; 109(9): 3510–3515.
  2. Eur J Neurosci. 2006 Mar;23(6):1417-26.
  3. PLoS One. 2012;7(5):e37080.
  4. Pharmacognosy Res. 2014 Jan;6(1):12-8.
  5. Phytother Res. 2010 Jun;24(6):859-63.
  6. Phytother Res. 2010 Oct;24(10):1567-74.
  7. Chem Pharm Bull (Tokyo). 2004 Nov;52(11):1358-61.

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