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Ground-breaking obesity drugs have transformed weight-loss treatment, and scientists are now investigating whether their effects could extend much further, potentially helping to protect the brain.
A new review published in Science examined growing evidence on how medications, including semaglutide and tirzepatide, may affect cognition and brain health.
The researchers, who spoke with Newsweek, found intriguing signs of potential benefits, but also a major unanswered question: Are these drugs acting directly on the brain, or is better brain health simply a consequence of improved metabolic health?
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Drugs such as semaglutide, the active ingredient in Wegovy and Ozempic, mimic the hormone GLP-1. Meanwhile tirzepatide, sold as Mounjaro and Zepbound, also targets another hormone pathway known as GIP.
These treatments produce substantial weight loss and improvements in cardiometabolic health.
That matters to 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 observational findings and results from clinical trials.
How GLP-1s May Affect Brain Health
Analyses of large patient datasets have associated GLP-1 receptor agonists with a reduced risk of cognitive impairment and dementia.
Animal studies have also suggested GLP-1-based treatments can influence learning and memory.
However, observational studies cannot establish that the drugs themselves caused the lower dementia risk.
Stina Börchers, the first author of the review and a researcher affiliated with the University of Gothenburg and the University of Copenhagen, told Newsweek 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 starting before significant damage occurs," Börchers said. "But how early, and when the window closes, is exactly what future trials need to answer."
When semaglutide was put to a more stringent test in people already living with early Alzheimer's disease, the picture changed.
In Novo Nordisk's EVOKE and EVOKE+ Phase 3 trials, semaglutide did not slow the clinical progression of Alzheimer's, despite producing changes in several disease-related biomarkers.
For Börchers and senior review author Christoffer Clemmensen, a research group leader at the University of Copenhagen, that discrepancy is particularly revealing.
"It shows that changing the biology of a disease isn't the same as changing its course," Börchers said. "What stood out to me was that the drug clearly did something: The biomarkers moved in the right direction, which is encouraging. But the effect was likely 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.
"Rather than closing the question, the result sharpens it: How can we make that effect stronger, and in whom?" Börchers said.
That apparent contradiction could prove important.
The review suggests obesity medicines may have greater potential for preserving cognitive abilities in people with obesity or Type 2 diabetes before significant cognitive problems become established, rather than reversing an existing neurodegenerative disease.
Dr. Shira Eytan, a board-certified endocrinologist in New York City who was not involved in the review, described the evidence for brain benefits as "promising, but not proven."
"The negative Alzheimer's trials do not rule out a potential preventive benefit, but they do mean we cannot assume one," Eytan told Newsweek. "Based on current evidence, brain protection alone is not a reason to start a GLP-1 medication. For someone who already has an indication such as obesity or Type 2 diabetes, any cognitive benefit remains a possibility, not a promise."
Reference
Börchers, S., Mazzini, G., Zetterberg, H. and Clemmensen, C. (2026). Obesity pharmacotherapies and cognition. Science, 394. doi:10.1126/science.aek9987
Contact Newsweek editors on this story: Kara Dolman and Shakeema Edwards.
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