Jason Karlawish is a physician and writer.
He researches and writes about issues at the intersections of bioethics, aging, and the neurosciences. He is the author of The Problem of Alzheimer’s: How Science, Culture, and Politics Turned a Rare Disease into a Crisis and What We Can Do About It and the novel Open Wound: The Tragic Obsession of Dr. William Beaumont. His essays have been published in The Wall Street Journal, The New York Times, Forbes, The Hill, The Los Angeles Times, The Philadelphia Inquirer, STAT, and The Washington Post. His STAT column Neurotransmissions examines the vast problem of dementia. A Professor of Medicine, Medical Ethics and Health Policy, and Neurology at the University of Pennsylvania, he is co-Director of the Penn Memory Center, where he cares for patients, and executive producer of the Age of Aging, a podcast that examines how to live well with an aging brain. He lives in Philadelphia.
Jason Karlawish writes STAT’s Neurotransmissions column
Listening to Ozempic….
“In the weeks leading up to Dec. 3, I imagined a fantastic headline: “Ozempic treats Alzheimer’s disease.”
On that day, at the CtAD 2025 meeting (CtAD stands for Clinical trials in Alzheimer’s Disease), in the Sapphire Ballroom of the Hilton San Diego Bayfront hotel, Novo Nordisk would present to the assembly of scientists and biopharma executives the results of its EVOKE studies, two clinical trials testing whether semaglutide treats people with early-stage symptomatic Alzheimer’s disease. Semaglutide is, of course, the chemical name for the brand Ozempic, FDA-labeled for the treatment of diabetes and to reduce the risk of major cardiovascular events, but widely known as the drug for obesity.
Widely known — that’s an understatement.
My imagination was animated because Ozempic is in a unique class of drugs. It is one of those drugs, like Prozac, whose name reaches deep into our collective consciousness. There, the word works on the imagination, evoking thoughts and stories about the experiences of patients on the drug. Their experiences’ deep meanings and wide implications transform how we talk and feel about the disease, the drug, and the patients who take it. Obesity — a stigmatized condition regarded by some as a visible surrender to gluttony — is manipulable by a drug, and that drug may affect a host of behaviors such as addiction. Matters of biology, free will, agency and culture are all thrown into a swirling debate over the causes of disease and how best to treat them. These kinds of drug aren’t simply treatments; they are iconic.
Sadly, my imagined headline remained a fantasy. Both EVOKE studies were negative. The curves charting the steady decline in persons on placebo or semaglutide were essentially identical. Seventy-eight weeks of daily treatment with 14 mg of oral semaglutide to beta-amyloid positive people with either mild cognitive impairment or mild stage dementia was no better than a daily placebo pill.
But what if the studies had been positive?
This question is, of course, entirely hypothetical, and yet, in this, the early years of the revolution in the diagnosis and treatment of dementia, I think it’s worth our attention. Someday we may have an iconic treatment, one that would unleash events that would propel this revolution, radically dividing time into before and after, like the shot heard round the world at Lexington and Concord or the cry of pain on the hilltop on Gethsemane. The progress that would ensue could be breathtaking. But it would come with long-simmering debates over how we ought to approach the vast problem of dementia.
Another reason to attend to these questions is that the EVOKE studies weren’t entirely negative. There were signals, target engagement, ambiguous hints that the drug might influence biomarkers of dementia. In a drug’s journey from bench to bedside, this is a vital event. We might not be done with Ozempic for Alzheimer’s. ...”
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