Cuproptosis and Immune Microenvironment Interplay in Temporal Lobe Epilepsy: Identification of Key Molecular Signatures and Therapeutic Targets

This study firstly establishes cuproptosis as a mechanistic bridge between copper dysregulation and TLE pathology, driving neuroinflammation via NF-κB and neuronal-glial dysfunction. The CRG-based subtyping offers novel disease classification, while CD44, PDE5A, and TUBA1A emerge as therapeutic targets to mitigate copper-mediated neurotoxicity. These findings reposition cuproptosis as a key pathway in epilepsy, providing a roadmap for precision therapy in drug-resistant TLE.