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We’ll learn about Ozempic’s potential for Alzheimer’s disease in 2025

Two later-stage trials investigating semaglutide, the drug in Ozempic, for treating Alzheimer's disease are due to complete in 2025, with potentially big results
B6DT04 Alzheimers disease. Series of computed tomography (CT) scans of an axial section through the head of a 74-year-old patient.
The brain shrinkage observed in Alzheimer’s may be prevented by semaglutide, the drug in Ozempic
ZEPHYR/Science Photo Library/Alamy

Ozempic and Wegovy are already transforming how we treat type 2 diabetes and obesity, and from next year another condition affecting millions of people worldwide might be added to the list: Alzheimer’s disease.

Two clinical trials investigating semaglutide, the drug in Ozempic and Wegovy, as a therapy for early Alzheimer’s are expected to conclude in 2025. If the results are positive, it could mark a breakthrough in treating this intractable condition.

Semaglutide belongs to a class of drugs that mimic a hormone called GLP-1. These GLP-1 agonists, as they are known, have wide-ranging effects, including regulating blood sugar, suppressing appetite and dampening inflammation. A growing body of evidence suggests that they may treat Alzheimer’s too.

The most compelling research is a small trial involving 204 people with mild to moderate Alzheimer’s. at Imperial College London and his colleagues found that one year of treatment with a daily injection of liraglutide, a GLP-1 agonist that is similar to semaglutide, slowed cognitive decline by 18 per cent compared with a placebo injection. The work, presented at the Alzheimer’s Association International Conference in July 2024, also showed the drug reduced brain shrinkage by about 50 per cent in areas vital for memory, learning and decision-making.

In another study published in October, at Case Western Reserve University in Ohio and her colleagues analysed health records from more than 1 million people with type 2 diabetes – which is considered a risk factor for Alzheimer’s – and found that those who were only prescribed semaglutide had a 67 per cent during the three-year study period than those who were only taking insulin.

It isn’t entirely clear why GLP-1 agonists appear to slow or even prevent Alzheimer’s. It could be through improving metabolic function in the brain, which is the ability of neurons to use glucose for energy, says at Brown University, Rhode Island. She notes that people with Alzheimer’s have impairments to their brain metabolism, which may contribute to their cognitive decline.

Other possible explanations include semaglutide reducing inflammation or improving risk factors associated with Alzheimer’s, such as type 2 diabetes, says Xu.

Results from the two later-stage trials that are – as confirmed by a spokesperson for Novo Nordisk, the pharmaceutical firm behind them – should help us uncover these mechanisms. Each includes roughly 1800 people with early Alzheimer’s who will have received either a daily tablet of semaglutide or a placebo for three years.

The main difference between the two trials is that in one of them, at least 20 per cent of the participants have small vessel disease, in which blood vessels in the brain narrow or become obstructed. Many people with Alzheimer’s also have small vessel disease, so this trial in particular will help us understand how semaglutide affects those who represent the general Alzheimer’s population, says at the Alzheimer’s Association in Chicago, Illinois.

Only two therapies – donanemab and lecanemab, two antibodies that remove sticky amyloid protein plaques from the brain – have ever been shown to slow the progression of Alzheimer’s. Yet their effect is modest and their high price, infusion delivery and risk of serious side effects have kept them out of reach for most people with the condition.

If semaglutide is shown to treat Alzheimer’s, we probably won’t have a use for these antibody drugs, says de la Monte. However, Edelmayer believes that they will remain a treatment option. Some people may respond better to one drug than another, she says. “We want this disease stopped in its tracks, so patients need options.”

Topics: Alzheimer's disease / Medical drugs