Two injections — and the end of Alzheimer's disease? It worked in mice
One of the main problems in treating Alzheimer's disease is that medicine is not yet able to restore already lost nerve cells. Even the most modern methods primarily try to slow down brain deterioration. American researchers claim they have found a fundamentally different approach: not only protecting surviving neurons but also making the brain create new ones. So far, this has only been achieved in mice, but the authors speak of a scientific breakthrough.

In Alzheimer's disease, a person gradually loses neurons and the connections between them. Hence — deterioration of memory, thinking, and the ability to perform ordinary daily tasks. Restoring already dead cells is extremely difficult. The adult brain has very limited abilities to form new neurons, so most existing approaches to treatment are aimed at preserving what still works for as long as possible.
As National Geographic Polska writes, a team of researchers from the University of South Carolina tried to take a different path. In an experiment on mice, scientists acted not directly on neurons, but on astrocytes, which usually perform auxiliary functions: supporting the work of nerve cells and participating in the regulation of their environment. But researchers were interested in their potential ability to transform into neurons.
Astrocytes are interesting because during embryonic development they can themselves transform into neurons. However, in an adult organism, this ability is blocked. One of the key factors that prevents such transformation is considered to be the PTBP1 protein.
A team of American scientists was able to make a diseased brain create new neurons by unblocking the ability of astrocytes to transform into nerve cells. For this, the researchers developed an injectable nanogel, Nano-ERASER, which destroys the PTBP1 protein.
Mice started building nests again
The method was tested on mice with an Alzheimer's disease model and detected cognitive impairments.
One of the indicative symptoms in such animals is the loss of the ability to build nests normally. For mice, this is normal behavior, so researchers use its impairment as one of the indicators of changes in brain functions.
Already after one injection, researchers noticed changes in the animals' behavior, and after two injections, the effect became even more pronounced. Within a few weeks, the mice started building nests again and performed significantly better in the water maze, which is used to test spatial memory in rodents.
Changes were also found during brain examination. According to the authors, after therapy, the inflammatory process and the number of pathological protein deposits decreased, while the density of healthy neurons increased.
Researchers attribute the improvement to the fact that after acting on PTBP1, some astrocytes acquired neuronal properties and integrated into neural networks. If this mechanism truly works as the authors believe, it represents a fundamentally important possibility: not only to stop the death of brain cells but also to try to compensate for the damage already inflicted.
Despite the promising results, the experiment should be treated with caution. It was previously reported that lowering PTBP1 levels could induce astrocytes to transform into neurons and even improve the condition of mice with a Parkinson's disease model. However, these results were not always reproducible.
The new study again yields encouraging results, but there is no guarantee yet that the method will work in humans. First, scientists plan to test its long-term effect and try it on primates.
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