New research suggests that soothing the brain’s immune cells could help prevent or reduce the harmful inflammation seen in Alzheimer’s disease.
The study points to the important role of norepinephrine—a brain chemical that also acts as a hormone—in controlling this inflammation.
These findings open the door to possible treatments that begin earlier and are better tailored to each person’s needs.
Norepinephrine is a key chemical messenger in the brain that affects nearly every type of brain cell. In diseases like Alzheimer’s, it has been shown to reduce inflammation.
According to Dr. Ania Majewska, a senior author of the study from the University of Rochester’s Del Monte Institute for Neuroscience, their research showed how boosting norepinephrine’s activity could protect the brain from early damage seen in Alzheimer’s.
The study was published in the journal Brain, Behavior, and Immunity and was carried out in mice.
It brought together two research teams focused on understanding how the brain’s immune system contributes to Alzheimer’s. Led by graduate student Linh Le, the researchers explored how norepinephrine affects tiny immune cells in the brain called microglia.
Microglia act like the brain’s clean-up crew and help maintain balance. One of their tools is a receptor called β2AR. This receptor lets them respond to norepinephrine and reduce inflammation.
But in Alzheimer’s, and with aging in general, this receptor becomes less active—especially in areas of the brain where damaging protein clumps called amyloid plaques start to form. As more plaques appear, nearby microglia lose more of these β2AR “calming” receptors, making it harder for them to control inflammation.
The team found that when they blocked or removed the β2AR receptor, the brain’s condition got worse. There were more plaques, more inflammation, and more damage to brain cells. But when they activated or boosted the receptor, the harmful effects decreased. Interestingly, the results depended on the timing of treatment and also differed between male and female mice.
This discovery shifts the way we think about Alzheimer’s. Until now, the disease was mainly seen as a buildup of plaques that kill brain cells. But this study shows that even before major damage appears, losing norepinephrine’s calming effect on microglia could already be making things worse.
This means future treatments might work better if they start earlier, perhaps even before symptoms begin.
Targeting the β2AR receptor in microglia could become a new strategy for Alzheimer’s treatment. Drugs that support this receptor could help microglia stay in an anti-inflammatory mode and protect brain function. Because the effects vary based on factors like sex and stage of disease, future treatments may also need to be personalized.
The research team included several scientists from the Del Monte Institute for Neuroscience, and their work adds valuable insight to the growing body of knowledge about how immune cells and inflammation affect brain health.
In short, helping the brain’s immune cells respond properly to norepinephrine could slow or change the course of Alzheimer’s disease—especially if treatment starts early and is adapted to each person.
If you care about Alzheimer’s disease, please read studies about the protective power of dietary antioxidants against Alzheimer’s, and eating habits linked to higher Alzheimer’s risk.
For more health information, please see recent studies that oral cannabis extract may help reduce Alzheimer’s symptoms, and Vitamin E may help prevent Parkinson’s disease.
The research findings can be found in Brain, Behavior, and Immunity.
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