Astrocytes Hold the Potential to Clear Alzheimer’s Plaques and Preserve Cognitive Function
Researchers at Baylor college of Medicine have discovered a natural mechanism that clears existing amyloid plaques in the brains of mouse models of Alzheimer’s disease and preserves cognitive function. The mechanism involves recruiting brain cells known as astrocytes,star-shaped cells in the brain,to remove the toxic amyloid plaques that build up in many Alzheimer’s disease brains.
Increasing the production of Sox9, a key protein that regulates astrocyte functions during aging, triggered the astrocytes’ ability to remove amyloid plaques. The study, published in Nature Neuroscience, suggests a potential astrocyte-based therapeutic approach to ameliorate cognitive decline in neurodegenerative disease.
“astrocytes perform diverse tasks that are essential for normal brain function, including facilitating brain communications and memory storage. As the brain ages, astrocytes show profound functional alterations; however, the role these alterations play in aging and neurodegeneration is not yet understood,” said first author Dr. Dong-Joo Choi, who was at the Center for Cell and Gene Therapy and the Department of Neurosurgery at Baylor while he was working on this project. Choi currently is an assistant professor at the Center for Neuroimmunology and Glial Biology, In
Astrocytes May Hold Key to Clearing Alzheimer’s Plaques, Restoring Cognitive Function
HOUSTON – Researchers at Baylor College of Medicine have discovered that boosting the activity of a protein called Sox9 in astrocytes – star-shaped cells in the brain – can enhance their ability to clear amyloid beta plaques, a hallmark of Alzheimer’s disease, and improve cognitive function in mouse models. The findings, published in Nature Neuroscience, suggest a potential new therapeutic avenue for combating the devastating neurodegenerative disease.
For years, the focus in Alzheimer’s research has been largely on neurons and the toxic buildup of amyloid beta plaques. However, astrocytes, once considered merely supportive cells, are now recognized as active players in brain health.This study highlights their crucial role in clearing debris, including the amyloid plaques associated with Alzheimer’s.
“We found that when we increased Sox9 levels in astrocytes, thay became more efficient at engulfing and breaking down amyloid beta plaques,” explains Dr. Choi. “This led to a meaningful reduction in plaque burden and, importantly, improved cognitive performance in the mice.”
The team observed that astrocytes with higher Sox9 levels exhibited increased expression of genes involved in phagocytosis – the process by which cells engulf and remove waste materials.This suggests that Sox9 acts as a master regulator, boosting the astrocytes’ natural cleaning capabilities.
Interestingly, the researchers found that Sox9 levels naturally decline with age, potentially contributing to the accumulation of amyloid plaques in the aging brain. This decline may explain why astrocytes’ natural ability to clean up could be just as critically important.
Choi, Deneen and their colleagues caution that more research is needed to understand how Sox9 works in the human brain over time. but their work opens the door to therapies that could one day harness the power of astrocytes to fight neurodegenerative diseases.
Sanjana Murali, Wookbong Kwon, Junsung Woo, Eun-Ah Christine Song, Yeunjung Ko, Debo Sardar, Brittney Lozzi, Yi-Ting Cheng, Michael R. Williamson, Teng-Wei huang, Kaitlyn Sanchez and joanna Jankowsky, all at Baylor College of Medicine, also contributed to this work.
More details:
Astrocytic Sox9 overexpression in Alzheimer’s disease mouse models promotes Aβ plaque phagocytosis and preserves cognitive function,Nature Neuroscience (2025). DOI: 10.1038/s41593-025-02115-w.
Astrocytes clear amyloid plaques and preserve cognitive function in Alzheimer’s mouse models (2025, November 21) retrieved 21 november 2025 from https://medicalxpress.com/news/2025-11-astrocytes-amyloid-plaques-cognitive-function.html. This document is subject to copyright. Apart from any fair dealing to private study or research, no part may be reproduced without the written permission. The content is provided for information purposes only.
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