Scientists have long known that Alzheimer’s disease is linked to sticky plaques and tangled proteins in the brain.
In recent years, they have also discovered that the brain’s blood vessels play an important role in how the disease progresses.
However, despite many advances, doctors still don’t have treatments that can fully stop or reverse the disease. One big reason is that we still don’t understand the exact chain of events that leads to brain cell damage.
Now, new research from Rockefeller University has found that two molecules—amyloid beta (Aβ) and fibrinogen—can form a toxic partnership that may be responsible for early damage in the brain. Amyloid beta is already known for forming the sticky plaques found in Alzheimer’s brains.
Fibrinogen is a common protein in blood that helps with clotting. On their own, these molecules don’t seem to cause major harm. But when they combine, they form clots that are hard to break down. These clots can lead to inflammation, damage blood vessels, a…
The research team, led by Dr. Erin Norris in the lab of Dr. Sidney Strickland, has been studying this Aβ/fibrinogen connection for nearly 20 years. In the past, their idea that blood vessel problems could be central to Alzheimer’s was seen as unusual. But now, more scientists are starting to believe that the vascular system plays a key role in the disease.
In their recent study, the team recreated small amounts of the Aβ/fibrinogen complex in the lab and tested it on mouse brain tissue and live mice. This allowed them to carefully observe what happens when the complex enters the brain.
They found that the complex caused a lot of damage. It harmed the connections between brain cells (called synapses), triggered inflammation, and caused leaks in the blood-brain barrier, which normally protects the brain from harmful substances in the blood.
To understand how important this interaction was, the researchers used special antibodies to block Aβ from attaching to fibrinogen. When they did this, the harmful effects were much less severe. This suggests that the complex itself is a key factor in the damage seen in Alzheimer’s.
One of the most important findings was that even tiny amounts of the Aβ/fibrinogen complex could cause damage—much more than either molecule could do alone. Mice that were exposed to the complex also showed higher levels of a marker called phospho-tau181.
This marker is used in humans to detect Alzheimer’s disease years before symptoms appear. This suggests that the harmful complex might play a role in the very early stages of the disease.
Using both brain slices and live animals helped the researchers be more confident in their findings. Seeing the same results in both tests shows that the Aβ/fibrinogen complex has powerful effects on the brain. The team now plans to study why the complex causes so much damage and how it might be stopped.
These findings are exciting because they suggest a new target for treatment. While Alzheimer’s is a complex disease with many causes, stopping the Aβ/fibrinogen complex might reduce some of the brain damage and work well alongside other therapies.
In short, this study brings us closer to understanding how Alzheimer’s disease begins and spreads. Blocking this one harmful interaction could be a helpful step toward better treatments and earlier prevention.
If you care about Alzheimer’s, please read studies about the likely cause of Alzheimer’s disease , and new non-drug treatment that could help prevent Alzheimer’s.
For more health information, please see recent studies about diet that may help prevent Alzheimer’s, and results showing some dementia cases could be prevented by changing these 12 things.
The study is published in Alzheimer’s & Dementia.
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