Sox9 overexpression in aging astrocytes protect against Alzheimer’s disease

How astrocytes contribute to Alzheimer’s disease pathogenesis is not yet clear although inflammation and reprogramming of astrocytes are common attributes.

The researchers show that Sox9 overexpression in astrocytes in AD mice models clears existing amyloid beta (Aβ) plaques and preserves cognitive function.

Mechanistically, Sox9 promotes the phagocytosis of Aβ plaques by astrocytes through the regulation of the phagocytic receptor MEGF10, which is sufficient to preserve cognitive function in AD models. 

These findings suggest that manipulating astrocytes could reverse the aging processes by altering homeostatic programs.

https://www.cell.com/trends/neurosciences/fulltext/S0166-2236(26)00048-2

https://sciencemission.com/Reprogramming-aging-astrocytes-in-AZ