The drug behind the blockbuster weight-loss drugs Ozempic and Vigovi doesn't slow cognitive decline in individuals with early-stage Alzheimer's, in keeping with two major recent studies. The findings close the door, for now, on the hope that treating diabetes and obesity could also help protect the brain.
OK and Ewc+ trials tracked nearly 3,800 people aged 55 to 85 with mild cognitive impairment or early Alzheimer's for 2 years. Those taking every day semaglutide did no higher than those given placebo on tests of memory, considering skills or every day functioning.
The drug used was Rebelsthe oral version of semaglutide will likely be prescribed for type 2 diabetes. Like Ozempic And Vagusit incorporates the identical lively ingredient.
Scientists had reason to be optimistic: before Lab work And studies in individuals with diabetes have suggested which will offer multiple ways to guard the brain, from calming inflammation to helping neurons work more efficiently.
These early indications didn't stop in patients. Despite inducing changes in some biological markers of the disease, the drug didn't slow overall cognitive decline.
The trials were global, randomized and placebo-controlled—the gold standard for drug testing in humans. The essential test they used was the Clinical Dementia Rating Scale, a rating that reflects each considering ability and the way well an individual manages on a regular basis tasks.
The researchers also examined the degrees of memory, behavior and Alzheimer's-related proteins within the cerebrospinal fluid. Although some biological markers improved barely in people taking the drug, their overall decline was no different from those on placebo.
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Scientists are enthusiastic about it GLP-1 Drugs like semaglutide because they appeared to tackle several processes involved in Alzheimer's.
the animal Studies They have been shown to cut back inflammation, improve how the brain responds to insulin, support the cell's “power stations” (mitochondria) and limit the build-up of amyloid plaques and tau tangles. Observational Studies In individuals with diabetes, it was even indicated that GLP-1 decreased more slowly in those on drugs.
GLP-1 is a hormone released after eating that helps regulate blood sugar. Semaglutide mimics this, stimulating the discharge of insulin, calming hunger signals and slowing digestion. In the brain, semaglutide prompts GLP-1 receptors on neurons and support cells, reducing inflammation, protecting cells from damage and helping them regulate energy and metabolism.
Lab Experiments It has also been shown to cut back the build-up of amyloid and tau. These overlapping effects make the semiglottide a robust candidate for Alzheimer's—but brain biology often behaves very in another way in real patients than in a petri dish or mice.
Why might it fail?
There might be several explanations for negative results. Treatment could come too late, as drugs that protect brain cells may fit best before symptoms appear.
Alzheimer's is a fancy disease, and targeting inflammation or metabolism itself once amyloid and tau have already developed. Also, changes in blood markers of disease don't all the time result in real-world improvements that patients or families can see, especially over just two years.
The safety of the drug has already been observed when used for diabetes or weight reduction. But with no sign of profit, Novo Nordisk is abandoning plans to increase the study for an additional yr. The full results will likely be shared at Alzheimer's conferences in 2026, giving researchers the prospect to dig into subgroups and extra findings that have not yet been released.
The headline findings provide vital answers but leave many details unclear. The researchers will need to see whether any subgroups of patients responded in another way, how stable the biological changes were, and whether any of the extra cognitive tests showed small effects.
For now, the message is obvious: promising biology doesn't guarantee a working cure. Semaglutide affects the processes related to Alzheimer's, but these trials show that it doesn't reduce symptoms once they begin. For families hoping for growth, it's one other reminder of how difficult it's to show experimental promise into real-world advantages.
The news led to a direct financial crisis. Novo Nordisk share price fell fastreflecting how much anticipation surrounds potential developments. The findings could also shape how pharmaceutical corporations conduct future trials of weight reduction and diabetes drugs for mental illnesses.
For now, though, semaglutide is unlikely to turn out to be a cure for Alzheimer's. Researchers might want to explore other strategies to see if the mechanisms observed in cells and mice can ever translate into meaningful cognitive advantages.