Similarly, in Alzheimer’s disease (AD), decreased SOCS3 might remove an essential regulatory constraint on STAT3, thereby increasing glial cell-mediated inflammation and accelerating disease progression (51).Future research should explore whether the SOCS3-STAT3 pathway represents a common inflammatory mechanism across these conditions, as identifying such a mechanism could provide a broad therapeutic target for intervention (52). This evidence concerns the gene STAT3 and early-onset autosomal dominant Alzheimer disease.