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Boosting Sox9 Reawakens Aging Astrocytes and Improves Memory in Alzheimer-like Mice

Researchers found that increasing the protein Sox9 in mice with Alzheimer-like pathology reactivated aging astrocytes, which upregulated the MEGF10 receptor and cleared amyloid‑beta plaques more effectively. Treated mice showed improved memory and behavior, while genetic loss of Sox9 worsened cognition and increased plaque burden. Although the work was done in mice, it highlights a potential complementary strategy: boosting the brain's own cleanup cells to combat neurodegeneration.

01:09 PM, 11/30/2025Health
Boosting Sox9 Reawakens Aging Astrocytes and Improves Memory in Alzheimer-like Mice

Researchers at Baylor College of Medicine report that increasing the transcription factor Sox9 restored waste‑clearing activity in aging astrocytes in mice engineered to develop Alzheimer-like pathology. Raising Sox9 increased expression of the MEGF10 receptor on astrocyte membranes, prompting these support cells to more effectively engulf and remove amyloid‑beta plaques. Treated mice showed improved performance on behavioral and memory tests, while genetic removal of Sox9 produced the opposite effects: worsened memory and greater plaque accumulation.

Key findings

  • Elevated Sox9 upregulated MEGF10 in astrocytes, enhancing their ability to clear amyloid‑beta plaques.
  • Sox9 augmentation improved cognition in mice that already had cognitive deficits and established plaques, suggesting a restorative effect on aging brain cells.
  • Deleting Sox9 impaired astrocyte function and accelerated plaque buildup and memory decline.

Context and caveats: These experiments were performed in mouse models, not humans. While amyloid‑beta plaques are a hallmark of Alzheimer’s, scientists continue to debate whether plaques are a primary cause or a downstream consequence of neurodegeneration. The findings nevertheless point to a promising complementary approach: boosting the brain's intrinsic cleanup machinery rather than targeting neurons or plaque formation alone.

Astrocytes perform diverse tasks that are essential for normal brain function, including facilitating neural communication and memory storage, said neuroscientist Dong‑Joo Choi (formerly at Baylor College of Medicine, now at the University of Texas Health Science Center at Houston). As the brain ages, astrocytes show functional changes; modest Sox9 enhancement appears to reinvigorate these cells.

The investigators also removed Sox9 genetically in a separate group of animals; those mice exhibited signs of astrocyte dysfunction, poorer memory recall, and increased amyloid accumulation. The study was published in Nature Neuroscience. The authors emphasize that further work is needed to test safety, to explore whether similar mechanisms operate in humans, and to determine how Sox9 or downstream targets such as MEGF10 could be harnessed therapeutically.

Implications: Enhancing Sox9 — or signaling pathways it controls — may offer a new, complementary strategy to support brain health by empowering astrocytes to clear toxic protein aggregates and protect neurons.

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