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Home Exclusive Mental Health Dementia

Ashwagandha extract boosts memory and cognition in people with mild cognitive impairment, study finds

by Eric W. Dolan
June 27, 2025
Reading Time: 4 mins read
[Adobe Stock]

[Adobe Stock]

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A new clinical trial published in the Journal of Psychopharmacology suggests that an extract of ashwagandha standardized with a compound called Sominone may improve memory and overall cognitive performance in people with mild cognitive impairment. Participants who took the supplement daily for two months showed significant improvements in several domains of memory and spatial reasoning compared to those who took a placebo. The supplement was also well-tolerated, with no significant side effects reported.

Mild cognitive impairment, or MCI, refers to a decline in memory or thinking skills that is noticeable but does not yet interfere significantly with daily life. People with MCI are at a higher risk of developing dementia later in life, including Alzheimer’s disease.

Currently, there are no approved medications specifically for treating MCI, and many people turn to lifestyle interventions such as exercise, diet changes, and cognitive training to slow cognitive decline. Herbal supplements have also gained attention, with ashwagandha — a plant long used in traditional Indian medicine — often recommended for stress, anxiety, and cognitive support.

Ashwagandha, also known by its botanical name Withania somnifera, has a long history of use in Ayurveda, the traditional medical system of India. Recent research has suggested that its compounds may have neuroprotective properties. In particular, Sominone — a metabolite derived from one of the plant’s active constituents — has shown promise in animal studies. It has been found to support the growth of nerve cells, protect neurons from damage, and enhance memory performance. The current study was designed to test whether a standardized extract of ashwagandha containing Sominone (called Somin-On™) could produce similar effects in humans diagnosed with MCI.

The researchers conducted a randomized, double-blind, placebo-controlled pilot study at a medical center in Jhansi, India. A total of 40 adults with MCI were selected to participate after meeting specific inclusion criteria. Participants were between the ages of 25 and 65 and had mild memory problems as measured by common clinical tests. They were randomly assigned to receive either 250 mg of Somin-Onâ„¢ or a placebo capsule once daily for 60 days. Both participants and researchers were unaware of who received the treatment and who received the placebo.

Cognitive function was measured using several standardized tools: the Montreal Cognitive Assessment (MoCA), the Mini-Mental State Examination (MMSE), the Wechsler Memory Scale-III (WMS-III), and the Shepard Mental Rotation Task. These assessments were administered at the beginning of the study, halfway through, and again at the end. The researchers focused on changes in immediate memory, general memory, working memory, attention, and visuospatial processing.

The results were striking. Compared to those taking a placebo, participants in the Somin-Onâ„¢ group showed consistent and statistically significant improvements across nearly all domains tested. Improvements were already evident after 30 days of treatment and became more pronounced by the end of the 60-day study period.

For example, the Shepard Mental Rotation Task, which assesses spatial reasoning and mental imagery, showed a 12% increase in performance at 30 days and a 32% increase at 60 days among those taking Somin-Onâ„¢, while the placebo group showed a decline by the end of the study. Similar trends were seen in the Wechsler Memory Scale.

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In measures of immediate memory, participants taking the supplement improved by about 7% at 60 days, while those in the placebo group actually declined slightly. General memory scores rose nearly 15% in the treatment group, compared to only a small increase in the placebo group. Working memory improved by over 18% in those taking Somin-Onâ„¢, with negligible change in the control group.

The two widely used screening tools, MoCA and MMSE, also showed marked improvement. MoCA scores in the treatment group rose nearly 15% from baseline, and MMSE scores increased by more than 19%. Both improvements were significantly higher than those observed in the placebo group.

The supplement was also well-tolerated. No participants in either group reported any adverse side effects, and standard blood tests and liver and kidney function markers remained stable throughout the trial.

The researchers suggest that the cognitive benefits of Somin-On™ may stem from its neuroprotective mechanisms. Previous animal research has shown that Sominone, the main active ingredient, can enhance the growth of neural connections and reverse memory deficits caused by damage to brain cells. It has also been shown to improve spatial memory and reduce brain cell shrinkage in models of Alzheimer’s disease, without necessarily affecting other markers like amyloid plaques. These findings hint at a potential mode of action involving the growth and maintenance of neural networks, rather than targeting traditional hallmarks of neurodegeneration.

Other possible mechanisms include increased resistance to oxidative stress, improvements in mitochondrial function, and support for cholinergic signaling — all of which have been linked to memory function in the brain. Inflammation and excitotoxicity, two processes involved in neurodegeneration, have also been shown to be reduced by components of ashwagandha in previous studies. Although the current study did not examine these mechanisms directly, the cognitive improvements observed may reflect the result of one or more of these biological pathways.

Despite these encouraging findings, the study has several limitations. First, the sample size was small, with only 40 participants. Larger studies are needed to confirm the results and better understand how widely they apply. Second, the duration of the study was limited to two months. It is unclear whether the benefits of Somin-Onâ„¢ persist over a longer period or whether the supplement could help prevent further decline. Third, the study did not use imaging techniques or biological markers to assess brain changes, so the underlying processes behind the cognitive improvements remain speculative.

Another limitation is the absence of an active comparator group. The study compared Somin-Onâ„¢ to a placebo, but did not compare it to other forms of ashwagandha or to other cognitive-enhancing treatments. Since ashwagandha contains multiple bioactive compounds, future studies could investigate whether Sominone alone is responsible for the observed benefits or if the effects arise from a broader mix of constituents.

The researchers suggest that future trials should include a more diverse participant pool, longer follow-up, and potentially integrate imaging or biomarker data to explore how ashwagandha affects brain structure and function. It would also be valuable to test the supplement in combination with other non-pharmaceutical interventions, such as cognitive training or physical exercise.

The study, “Effect of ashwagandha (Withania somnifera) extract with Sominone (Somin-Onâ„¢) to improve memory in adults with mild cognitive impairment: A randomized, double-blind, placebo-controlled study,” was authored by Hari Prakash Rai and Deo Nidhi Mishra.

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