A groundbreaking study from Northwestern University suggests that Alzheimer’s disease may be stopped before memory loss begins, offering new hope for millions at risk of the devastating condition. Researchers have identified a previously unknown, highly toxic protein that appears to trigger Alzheimer’s disease decades before symptoms emerge and demonstrated that an experimental drug can block this early damage in animal models.
Alzheimer’s disease has long been associated with the accumulation of amyloid beta plaques in the brain. However, the new research shifts attention to a more dangerous culprit: a specific subtype of amyloid beta oligomers, small clusters of toxic proteins, that appear very early in the disease process. This newly identified subtype accumulates inside neurons and nearby astrocytes, the brain’s support cells, initiating inflammation and neuronal dysfunction long before cognitive decline becomes noticeable.
The study, published in Alzheimer’s & Dementia, investigated the effects of an experimental small-molecule drug called NU-9. Researchers administered NU-9 to mice genetically predisposed to Alzheimer’s disease before any symptoms appeared. After 60 days of treatment, the drug dramatically reduced toxic amyloid beta oligomers, suppressed neuroinflammation, and decreased reactive astrogliosis, an inflammatory response linked to early disease progression
Notably, NU-9 also reduced abnormal levels of TDP-43, a protein associated with several neurodegenerative diseases and cognitive impairment. These improvements were observed across multiple brain regions, suggesting that the drug has a broad, brain-wide anti-inflammatory effect.
According to the researchers, Alzheimer’s pathology begins many years before memory loss becomes evident, which may explain why many clinical trials have failed. Most treatments are tested only after symptoms appear, when irreversible brain damage has already occurred. By targeting the disease in its earliest, pre-symptomatic stage, NU-9 represents a shift toward prevention rather than late-stage treatment
The findings also support a growing emphasis on early diagnosis. Scientists note that blood-based biomarkers for Alzheimer’s are currently under development, raising the possibility that individuals at risk could be identified early and treated proactively. Researchers liken this approach to managing high cholesterol to prevent heart disease—intervening early to reduce long-term risk
While NU-9 has already received FDA clearance for human trials in amyotrophic lateral sclerosis (ALS), further studies are needed before it can be tested clinically for Alzheimer’s disease. Ongoing research will examine the drug’s long-term effects, its impact on memory and cognition, and its effectiveness in models of late-onset Alzheimer’s that more closely resemble human aging
If future trials confirm these findings in humans, NU-9 could mark a breakthrough, transforming Alzheimer’s from an untreatable condition into a preventable disease detected and halted before memory loss begins.