Brain Cell Rejuvenation Shows Promise in Alzheimer’s Mouse Model
HOUSTON, TX - Scientists at Baylor College of Medicine have identified a potential new therapeutic target for Alzheimer’s disease: boosting a single protein to revitalize aging brain cells and improve memory function in mice. The study, published in Nature Neuroscience, suggests that enhancing the natural cleanup abilities of astrocytes - star-shaped cells in the brain - could be as important as targeting amyloid plaques, a hallmark of the disease.
Researchers found that increasing levels of the protein REST in astrocytes restored their youthful function, leading to improved cognitive performance in mice already exhibiting alzheimer’s-like symptoms.As mice with elevated REST levels performed better on memory tests, researchers observed a reduction in the negative impact of amyloid-beta clumps on synapses.
“An important point of our experimental design is that we worked with mouse models of Alzheimer’s disease that had already developed cognitive impairment, such as memory deficits, and had amyloid plaques in the brain,” explains researcher Choi. “We believe these models are more relevant to what we see in many patients with Alzheimer’s disease symptoms than other models in which these types of experiments are conducted before the plaques form.”
Alzheimer’s disease affects millions worldwide, and despite ongoing research, effective treatments remain elusive. While many approaches focus on neurons or preventing amyloid plaque formation, this study highlights the crucial role of astrocytes in maintaining brain health.
“Most current treatments focus on neurons or try to prevent the formation of amyloid plaques,” says neuroscientist Benjamin Deneen. “This study suggests that enhancing astrocytes’ natural ability to clean up could be just as important.”
The findings offer a new avenue for Alzheimer’s research, though scientists caution that further investigation is needed to determine if similar results can be achieved in humans. There are multiple strategies being explored to clear amyloid-beta clumps or prevent their formation, but the fundamental question of whether these protein aggregations cause Alzheimer’s or are a result of the disease remains unanswered.
