Protein deposits in the brain are common in many neurodegenerative diseases.
These harmful proteins, like tau, make nerve cells die and cause parts of the brain to shrink.
This can lead to dementia, a condition that gradually makes people lose their memory and other important mental functions.
Diseases like Alzheimer’s and frontotemporal dementia are closely linked to these protein deposits.
The Role of Serotonin and 5-HT7R
Professor Dr. Evgeni Ponimaskin from the MHH Institute of Neurophysiology and his team have found a key link in this process. They found a specific serotonin receptor, named 5-HT7R, plays a big part.
What’s serotonin? It’s a messenger substance, kind of like a mail carrier in your body.
It manages many important tasks like helping your blood clot, learning, and controlling your sleep. It’s also known as the “happiness hormone” because it helps control our mood.
The 5-HT7R receptor is special because it’s always active. It helps to create a chemical change in tau proteins, which leads to their buildup in cells.
But it turns out that the receptor’s overactivity can be stopped, using what scientists call inverse agonists.
Antipsychotic Drug Shows Promise
Now, this is where it gets exciting. The team found that an antipsychotic drug, amisulpride, can block the 5-HT7R receptor. By blocking this receptor, the drug stops the harmful tau protein from building up.
Amisulpride is not new. It’s already used to treat schizophrenia, a mental disorder that affects how a person thinks, feels, and behaves. But now, it might also be used to treat dementia.
This drug has been tested on cell models and in animal models of dementia, and the results were promising. The researchers published these results in a journal called Alzheimer’s & Dementia.
From Lab to Clinic
Although the substance class of inverse agonists has been patented for dementia treatment, up until now, it could only be used in labs, not in real patients.
So, the scientists looked at drugs that were already approved and could possibly influence the serotonin receptor as a side effect.
Amisulpride stood out because it was a strong 5-HT7R receptor agonist. While it can’t repair dead nerve cells, it could possibly slow down dementia or even prevent it if caught early enough.
They even found that amisulpride had a therapeutic effect on human stem cells with disease-relevant mutations.
Upcoming Clinical Trials
Excitingly, the next step is to start a Phase II clinical trial. This is a type of study where a drug is given to people to see how well it works and if it’s safe.
Professor Ponimaskin, in collaboration with other scientists and institutions, is preparing for this trial, aiming to start it by the end of this year.
They want to test amisulpride’s effect on patients with dementia. If successful, this could bring us one step closer to an effective treatment for dementia.
If you care about dementia, please read studies about Vitamin B9 deficiency linked to higher dementia risk, and flavonoid-rich foods could help prevent dementia.
For more information about brain health, please see recent studies that cranberries could help boost memory, and these antioxidants could help reduce dementia risk.
The study was published in Alzheimer’s & Dementia.
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