Experimental molecule may be a potent weapon against Alzheimer’s
January 07, 2026
The NU-9 molecule may one day delay or even prevent the destruction of neurons that begins decades before the first symptoms of Alzheimer’s disease appear
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You think you’re fine. Your family and friends think you’re fine. But, just maybe, you’re not. Maybe you already have Alzheimer’s disease, but you just don’t know it yet, because it can begin destroying your brain decades before anyone even suspects.
According to Alzheimer’s Disease International, about 55 million people around the world were living with dementia in 2020, with 10 million new cases each year, meaning a new one arising about every three seconds. The disease’s economic impact is massive – about $US818 billion in 2015, and about $1.3 trillion today.
But the personal cost is beyond any economic price.
Seeing one’s spouse of decades, or one’s siblings or parents of a lifetime lose contact with all their yesterdays and even their todays, slowly being stripped of reason, self-control, personality, and even the ability to take care of basic physical needs, is a massive burden that disproportionately falls on the shoulders of women as caregivers, and which yields the “reward” of depression and anxiety. In other words, Alzheimer’s profoundly wounds not just the diagnosed individuals, but their families.
That’s why a new study from Northwestern University offers so much hope, because if researchers there are correct, their new small-molecule NU-9 drug may be able to stop Alzheimer’s disease long before it begins ruining lives.
“Alzheimer’s disease begins decades before its symptoms appear,” says Daniel Kranz, lead author of a paper that was recently published in Alzheimer’s and Dementia: The Journal of the Alzheimer’s Association. Long before diagnosis or even suspicion of the disease’s manifestation, Kranz says toxic amyloid beta oligomers have begun “accumulating inside neurons and glial cells becoming reactive long before memory loss is apparent.”
That long period in which Alzheimer’s disease is performing silent neurological sabotage in which “the underlying pathology is already advanced,” means that clinical trials likely fail because for most patients “they start far too late,” says Kranz, a recent PhD graduate in Interdisciplinary Biological Sciences at Northwestern’s Weinberg College of Arts and Sciences. “In our study,” he says, “we administered NU-9 before symptom onset, modeling this early, pre-symptomatic window.”
Research into NU-9 isn’t new.
About 15 years ago, key co-author Richard Silverman (who is also the Patrick G. Ryan/Aon Professor in Weinberg’s Department of Chemistry) invented the drug after having already invented pregabalin (Lyrica) to treat fibromyalgia, nerve pain, and epilepsy. With Kranz and corresponding author William Klein (an Alzheimer’s disease expert and a professor of neurobiology at Weinberg), Silverman and colleagues worked for years to find or create a small molecule to prevent the aggregation of neurodegenerative proteins.
By 2021, the team proved the efficacy of NU-9 (which Silverman’s company Akava Therapeutics now manufactures as AKV9) using animal models for amyotrophic lateral sclerosis (ALS). By removing the destructive SOD1 and TDP-43 proteins, the drug revitalized upper motor neurons, and in 2024 NU-9 received clinical trial approval to treat ALS from the US Food and Drug Administration.
Then, early in 2025, Silverman’s team proved that when applied to the hippocampus (a brain region that enables memory and thus learning), NU-9 could remove toxic amyloid beta oligomers in lab-grown brain cells.
“Cells have a mechanism to get rid of these proteins,” says Klein, cofounder of Acumen Pharmaceuticals, which is clinically testing its therapeutic monoclonal antibody against a highly toxic sub-species of amyloid beta oligomers that may cause neuronal dysfunction, inflammation, and activation of immune cells. While the cell mechanism that can fight these proteins “gets damaged in degenerative diseases like ALS and Alzheimer’s,” says Klein, “NU-9 is rescuing the pathway that saves the cell.”
Preventing dementia would ultimately liberate not only trillions of dollars from providing medical treatment and home care, but offer the opportunity to redirect trillions of person-hours of suffering, loneliness, anxiety, and depression into maintaining and improving quality of life for individuals, families, and communities.
Source: Northwestern University
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