Lowering RTP801 in brain cells may ease memory loss in Alzheimer’s disease.
Scientists in Spain are making progress in understanding what happens inside the brain during Alzheimer’s disease, and their latest findings may help shape future treatments. A team from the University of Barcelona has zeroed in on a protein that plays a key role in the thinking and memory problems that come with the illness. This protein, known as RTP801, seems to get in the way of healthy brain activity when it shows up in certain support cells in the brain. These findings, though based on studies in mice, offer a fresh look at what might be going wrong and how we might try to fix it.
Alzheimer’s is a disease that slowly damages memory and thinking. For a long time, scientists have focused on two main signs of the disease: sticky clumps called amyloid plaques that form outside nerve cells, and twisted proteins called tau that gather inside them. These changes are harmful, but they don’t tell the whole story. Researchers are now looking at how other parts of the brain, especially non-nerve cells, might also play a part. That’s where astrocytes come in.
Astrocytes are star-shaped cells that support and protect the brain. For years, they were seen as background players—important, but not active participants in how the brain works. Now that view is changing. These cells help control the balance of brain signals and respond to injury. In Alzheimer’s, they become more active in a way that’s not helpful, sometimes making the situation worse. The research team in Barcelona has shown that the RTP801 protein may be one of the reasons astrocytes become harmful.
By lowering the levels of RTP801 in these support cells in mice with signs of Alzheimer’s, the scientists noticed some surprising changes. The animals had better memory and more normal patterns of brain activity. That’s a big deal because one of the key problems in Alzheimer’s is that the brain’s network of signals becomes overactive and disorganized, which affects thinking and mood. When RTP801 was reduced, brain connections looked more like those in healthy brains.
Another important finding was related to a chemical in the brain called GABA. This chemical helps slow things down and keeps brain activity in check. In Alzheimer’s, GABA levels drop, which can lead to overstimulation. The team found that by targeting RTP801, they could bring GABA levels back up—at least partially. This suggests that RTP801 not only causes trouble in astrocytes but might also be linked to the loss of certain nerve cells that make GABA.
These particular nerve cells, known as PV+ interneurons, help keep the brain’s rhythm steady. Losing them can throw everything off balance. The researchers think that too much RTP801 might damage these cells. When they reduced the protein, some of these neurons started to recover, and that seemed to help the overall health of the brain in their test animals.
While these results are early and based on animal studies, they open the door to exploring new treatment ideas. If RTP801 is playing a big role in the changes that lead to memory problems, calming brain overactivity, and harming important nerve cells, then learning how to safely lower its levels could be helpful. More studies are needed to figure out if the same results would happen in people, and if they do, how best to apply this knowledge.
For now, this work adds another piece to the Alzheimer’s puzzle. It shifts the spotlight toward lesser-known parts of the brain and how they might be part of the problem—and possibly the solution. It gives scientists a new path to follow as they continue searching for ways to protect the brain and slow the course of this disease.
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Study uncovers new molecular mechanisms linked to Alzheimer’s cognitive decline
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