Discovery of a promising molecule in the treatment of Alzheimer’s disease

Researchers have discovered a new molecule that opens the way for a new treatment for Alzheimer’s disease, which is defined as a progressive neurological disorder that leads to brain atrophy and the death of its cells.
Alzheimer’s disease is the most common cause of dementia, which is a persistent decrease in thinking, behavioral and social skills that affects a person’s ability to function independently.
This disease affects millions of people around the world. Hence, the large number of studies that study it in an attempt to contain it.
Alzheimer’s disease usually starts slowly and then gets progressively worse. The first symptom is usually difficulty remembering recent events, which is often described as forgetfulness.
As the disease progresses, symptoms can include confusion, irritability, aggressiveness, mood swings, language problems, and long-term memory loss. And with an aging population, the fight against this devastating disease has never been more urgent. Recently, a team of researchers discovered a new potential weapon against Alzheimer’s disease.
Building on the current knowledge that microRNA-212-3p, denoted miR-212-3p, can play a role in fighting Alzheimer’s disease, a research team conducted a series of rigorous experiments to explore how it works. that. The findings suggest that increased levels of the molecule miR-212-3b in the brain may help control inflammation, which is a major player in Alzheimer’s disease. These findings light a beacon of hope for patients and their families and offer an exciting avenue for potential future therapies.
The research findings have been published in the Bosnian Journal of Basic Medical Sciences.
MicroRNA, inflammation, and Alzheimer’s disease
MicroRNAs, including miR-212-3b, are small molecules found in cells that play a critical role in controlling the activities of specific genes. Our genes are the blueprint for every protein in our bodies. By controlling them, microRNAs such as miR-212-3b help keep our bodies functioning properly.
Inflammation is part of the body’s natural defense mechanism, but in Alzheimer’s disease, this protective response gets out of control and ends up damaging brain cells, contributing to cognitive decline and memory loss.
The team behind this study wanted to understand whether miR-212-3b could help control this harmful inflammation. Thus, fighting Alzheimer’s disease.
To test their theory, the team conducted a series of rigorous experiments. They began by injecting a compound called Aβ1-42, which is known to cause Alzheimer’s-like symptoms, into mice. They then artificially increased the levels of miR-212-3p in the brains of some of these mice, while others served as control groups.
Exciting discovery: miR-212-3b improves memory and learning
The results were promising. Mice with elevated miR-212-3b levels showed improved learning and memory abilities, a sign that increased miR-212-3p may be able to reverse some of the effects of the disease. This is significant because it is the first time that miR-212-3b has been shown to have such a positive effect.
Building on these positive results, the researchers also found that increasing miR-212-3p reduced levels of inflammation in the brains of mice. High levels of inflammation are a known driver of Alzheimer’s disease. Therefore, these results indicate that enhancing miR-212-3p could provide a new approach to addressing this deleterious inflammation. Thus, slowing down or even preventing the progression of Alzheimer’s disease.
Deeper understanding:
To understand how miR-212-3b achieves these impressive benefits, the team delved into the molecular mechanism of brain cells. They discovered that miR-212-3b interacts with two other molecules, SP1 and beta-secretase 1 (BACE1), effectively reducing their activity.
SP1 and BACE1 are part of the proinflammatory pathway in the brain and are known to be overactive in Alzheimer’s patients. By blocking their activity, miR-212-3b can help control harmful inflammation in the brain, protecting brain cells from harm.
The team confirmed these findings with further experiments in cell cultures, strengthening evidence of the role of miR-212-3p in controlling inflammation.
Impacts and future directions
The results showed the potential therapeutic role of miR-212-3b against Alzheimer’s disease. By showing that this molecule can control inflammation in the brain and improve memory and learning in mice, the research provides a promising avenue for developing new treatments for this disease.
“Our research provides a new understanding of how miR-212-3b plays a role in controlling inflammation, which plays a major role in Alzheimer’s disease,” said study lead author Wei Nong of Guangxi University of Chinese Medicine in Nanning, Guangxi Province, China. “It is the first step towards harnessing this.” molecule for future therapy.
Although these results are promising, more research is needed. The researchers used a mouse model of Alzheimer’s disease and human cell cultures in their study. These are well-established research methods, but more research will be needed to confirm these findings in people with Alzheimer’s disease.
For example, a critical next step will be to investigate miR-212-3b levels in patients with Alzheimer’s disease compared to healthy individuals.
“The journey to a potential new treatment for Alzheimer’s disease is long, and we are still in the early stages,” said Dr. Chiquan Wei of Guangxi University of Chinese Medicine. “Our study is a promising start, but we need to do more research to understand the full potential of miR-212-3b.” “.
While we are still far from a cure for Alzheimer’s disease, this study highlights a potential new path to treatment. By understanding how miR-212-3b works inside the brain, researchers are paving the way for new therapies that could slow or even stop the progression of Alzheimer’s disease.

#Discovery #promising #molecule #treatment #Alzheimers #disease


Posted

in

by

Comments

Leave a Reply

Your email address will not be published. Required fields are marked *