For many years, Alzheimer’s disease has remained one of the most difficult brain disorders to treat. Doctors often diagnose it only after memory problems and confusion begin to interfere with daily life.
By that point, the damage inside the brain is already severe, and treatments have very limited effects. Now, a new study from Northwestern University suggests that an experimental drug might help stop Alzheimer’s much earlier, before these symptoms ever appear.
Alzheimer’s disease does not begin with forgetfulness. Instead, it starts quietly, sometimes decades earlier, with tiny harmful changes inside brain cells. One of the earliest problems involves amyloid beta, a protein that can clump together in abnormal ways.
These small clusters, called oligomers, are more harmful than the larger plaques that appear later in the disease. Scientists have known about amyloid beta for many years, but exactly which forms are most dangerous has remained unclear.
In this new research, scientists discovered a previously unknown and highly toxic type of amyloid beta oligomer. This specific form appears very early in the disease and seems to trigger several damaging events in the brain.
These include problems with nerve cell function, long-lasting inflammation, and the activation of immune cells in the brain. Together, these changes slowly weaken and destroy brain cells over time.
The researchers tested an experimental drug called NU-9, which is a small chemical compound taken by mouth. When given to mice that were genetically programmed to develop Alzheimer’s disease, NU-9 sharply reduced the amount of this toxic amyloid beta subtype.
More importantly, it greatly reduced the damage that usually follows. The mice received the drug before showing any memory problems, which allowed the scientists to study its effects during the earliest stage of the disease.
NU-9 was originally designed many years ago as part of a long effort to stop harmful protein buildup in brain diseases. Earlier studies showed that it worked in animal models of ALS, another serious condition caused by toxic proteins.
In those studies, NU-9 helped clear damaging proteins and restore nerve cell health. Because of these results, the drug has already been approved to begin human trials for ALS.
More recently, scientists discovered that NU-9 could also help in Alzheimer’s disease. In earlier experiments using brain cells grown in the lab, the drug successfully cleared toxic amyloid beta clusters from cells in the hippocampus, a brain region essential for learning and memory.
In the newest study, researchers wanted to know if NU-9 could stop the disease process even earlier. They treated mice that had not yet developed symptoms with daily doses of the drug for two months.
The results were remarkable. NU-9 greatly reduced inflammation in the brain, especially a process involving astrocytes. Astrocytes are star-shaped support cells that normally protect nerve cells, but when they become overly active, they release harmful signals that damage the brain.
The study showed that NU-9 prevented astrocytes from entering this harmful state. It also reduced abnormal forms of another protein called TDP-43, which is often linked to brain cell damage and thinking problems. These improvements were seen across multiple brain regions, suggesting that the drug has widespread protective effects.
While studying these changes, the researchers made another major discovery. They identified a specific subtype of amyloid beta oligomer that appears inside stressed nerve cells early in the disease and then moves onto nearby astrocytes.
When this toxic form attaches to astrocytes, it may trigger a wave of inflammation that spreads through the brain long before memory loss begins. The researchers believe this subtype may act as an early spark that sets Alzheimer’s disease in motion.
NU-9 was especially effective at reducing this toxic subtype. By lowering it, the drug may stop astrocytes from becoming destructive in the first place. This is important because once astrocytes turn harmful, they damage connections between brain cells, release inflammatory substances, and speed up brain degeneration.
The researchers compare this approach to preventing heart disease. High cholesterol does not cause immediate symptoms, but doctors treat it early to prevent future heart attacks. In a similar way, NU-9 could one day be used in people who show early signs of Alzheimer’s disease through blood tests or other markers, long before memory problems appear.
Several early blood tests for Alzheimer’s are currently being developed. If such tests become widely available, a drug like NU-9 could be used as a preventive treatment to slow or possibly stop the disease before it causes lasting damage.
The research team is now testing NU-9 in additional Alzheimer’s models, including forms that better reflect normal aging in humans. They also plan to study treated animals over longer periods to see whether memory remains intact and whether brain cells stay healthy over time.
When reviewing and analyzing these findings, the study stands out because it focuses on the earliest stage of Alzheimer’s disease rather than trying to reverse damage that has already occurred. Many past clinical trials have failed because treatments were given too late.
By identifying a specific toxic protein subtype and showing that it can be reduced before symptoms appear, this research offers a clear and logical new direction.
While the results are still limited to animal studies and more testing is needed in humans, the findings provide strong evidence that early intervention could dramatically change how Alzheimer’s disease is treated in the future.
If you care about Alzheimer’s disease, please read studies that bad lifestyle habits can cause Alzheimer’s disease, and strawberries can be good defence against Alzheimer’s.
For more information about brain health, please see recent studies that oral cannabis extract may help reduce Alzheimer’s symptoms, and Vitamin E may help prevent Parkinson’s disease.
The study is published in Alzheimer’s & Dementia.
Copyright © 2025 Knowridge Science Report. All rights reserved.
