Key Points:
- Alzheimer’s prevention: NU-9, a drug from Northwestern University, may stop early Alzheimer’s changes before memory loss begins.
- It reduces toxic proteins and brain inflammation, protecting neurons in mice.
- The study highlights prevention, but human trials are still needed.
Scientists at Northwestern University report a new experimental drug slowed or prevented early Alzheimer’s brain changes in mice, raising hopes for treatments that could advance Alzheimer’s prevention before memory loss begins.
Scientists at Northwestern University are developing an experimental drug that could change how Alzheimer’s disease is treated by targeting the illness years before symptoms appear.
The drug, known as NU-9, showed strong effects in laboratory tests on mice by reducing early brain damage linked to Alzheimer’s, according to a recent study conducted by the university’s researchers.
Alzheimer’s develops gradually, often decades before diagnosis. Early damage is driven by small clusters of toxic proteins that quietly disrupt brain cells long before memory or thinking problems emerge.
Drug Targets Alzheimer’s at Its Earliest Stage
Researchers said NU-9 focuses on the earliest biological changes associated with Alzheimer’s, rather than treating symptoms after the disease has progressed.
“Alzheimer’s does not begin with memory loss. It begins with subtle molecular changes in the brain,” the researchers said in findings released with the study.
The study identified a previously unknown subtype of amyloid beta oligomers, toxic protein clusters believed to play a key role in triggering early inflammation and nerve cell damage.
Scientists found this subtype to be especially harmful during the initial stages of Alzheimer’s, making it a promising target for Alzheimer’s prevention.
Mouse Study Shows Reduced Brain Damage
When NU-9 was administered to mice showing early Alzheimer’s-like changes, researchers observed a significant reduction in brain inflammation and toxic protein buildup.
The drug helped protect neurons from damage and preserved normal brain function, the study reported.
“By reducing this toxic protein subtype, NU-9 prevented much of the damage we typically see at the start of the disease,” the researchers said.
The treatment also lowered levels of TDP-43, another harmful protein linked to memory loss and cognitive decline in Alzheimer’s and other neurodegenerative disorders.
TDP-43 is associated with more severe disease progression, and its reduction suggests NU-9 may have broader protective effects in the brainfurther supporting Alzheimer’s prevention strategies.
Focus Shifts to Prevention, Not Cure
Experts say the findings highlight a growing shift in Alzheimer’s research toward prevention rather than late-stage treatment.
“Stopping the disease before symptoms appear could be the most effective strategy we have,” the researchers said, cautioning that the drug has so far only been tested in animals.
The study does not mean a cure is imminent. Human clinical trials are still needed to determine whether NU-9 is safe and effective in people.
Still, scientists say the results provide strong evidence that targeting early molecular changes could delay or even prevent Alzheimer’s altogether.
Alzheimer’s affects millions worldwide and has no cure. Current treatments offer limited symptom relief but do not stop the disease from progressing.
Researchers emphasized that early intervention remains the key challenge, as most patients are diagnosed only after significant brain damage has already occurred.
The Northwestern team said further research will focus on advancing NU-9 toward human trials and refining methods to detect Alzheimer’s before symptoms appear, marking an important step forward in Alzheimer’s prevention research.
