Breakthrough obesity drugs have transformed weight loss treatments, and scientists are now investigating whether their effects could extend much further, potentially helping to protect the brain.
A new review published in Science reviewed growing evidence on how medications, including semaglutide and tirzepatide, may affect cognition and brain health.
The researchers, who spoke with News weekfound intriguing signs of potential benefits, but also a major unanswered question: Do these drugs act directly on the brain, or is better brain health simply a consequence of better metabolic health?
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Drugs such as semaglutide, the active ingredient in Wegovy and Ozempic, mimic the GLP-1 hormone. Meanwhile, tirzepatide, sold under the names Mounjaro and Zepbound, also targets another hormonal pathway known as GIP.
These treatments result in substantial weight loss and improvements in cardiometabolic health.
This is important for the brain because obesity, type 2 diabetes, and vascular dysfunction are all associated with cognitive impairment and dementia, while insulin resistance and chronic inflammation provide possible biological links between metabolic and brain health.
What particularly stands out is the contrast between the observational results and the results of clinical trials.
How GLP-1 can affect brain health
Analyzes of large patient data sets have associated GLP-1 receptor agonists with a reduced risk of cognitive impairment and dementia.
Animal studies have also suggested that GLP-1 treatments may influence learning and memory.
However, observational studies cannot establish that the medications themselves cause a lower risk of dementia.
Stina Börchers, first author of the review and an affiliated researcher at the University of Gothenburg and the University of Copenhagen, said: News week that it is not yet clear who might ultimately benefit.
“The most plausible candidates are people with obesity or type 2 diabetes, whose cognitive problems are linked to treatable factors like blood sugar, blood pressure, vascular health and sleep,” she said.
Timing could also prove crucial. “Any benefit may depend on getting started before significant damage occurs,” Börchers said. “But when and where the window closes is exactly what future trials will need to answer.”
When semaglutide was subjected to more rigorous testing in people who already had early-stage Alzheimer’s disease, the situation changed.
In Novo Nordisk’s Phase 3 EVOKE and EVOKE+ trials, semaglutide did not slow the clinical progression of Alzheimer’s disease, despite changes in several disease-related biomarkers.
For Börchers and the review’s lead author Christoffer Clemmensen, head of a research group at the University of Copenhagen, this discrepancy is particularly revealing.
“This shows that changing the biology of a disease is not the same as changing its evolution,” Börchers said. “What struck me was that the drug clearly did something: the biomarkers moved in the right direction, which is encouraging. But the effect was probably too small.”
She noted that semaglutide lowered markers of nerve cell damage by about 10 percent, compared with about 30 percent for drugs that have been shown to slow Alzheimer’s disease.
“Rather than closing the question, the result makes it more precise: how can we make this effect stronger, and in whom?” » said Borchers.
This apparent contradiction could prove important.
The analysis suggests that anti-obesity drugs may have greater potential to preserve the cognitive abilities of people with obesity or type 2 diabetes before significant cognitive problems set in, rather than reversing an existing neurodegenerative disease.
Dr. Shira Eytan, a board-certified endocrinologist in New York City who was not involved in the study, described the evidence for brain benefits as “promising, but unproven.”
“The negative Alzheimer’s trials don’t rule out a potential preventive benefit, but they mean we can’t assume one,” Eytan said. News week. “Based on current evidence, brain protection alone is not a reason to start taking a GLP-1 drug. For someone who already has an indication such as obesity or type 2 diabetes, any cognitive benefit remains a possibility and not a promise.”
Reference
Börchers, S., Mazzini, G., Zetterberg, H. and Clemmensen, C. (2026). Pharmacotherapies of obesity and cognition. Science, 394. doi:10.1126/science.aek9987
Contact Newsweek editors on this story: Kara Dolman and Shakeema Edwards.
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