The Role of Immune Cell Subsets in the Development of Postoperative Cognitive Dysfunction in Surgical Patients under Anesthesia.

Abstract

Background: Postoperative cognitive dysfunction (POCD) affects 10-54% of surgical patients, especially the elderly. It is increasingly recognized as a major perioperative complication driven by neuroinflammatory mechanisms. While physiological postoperative inflammation supports wound healing and recovery, pathological hyperactivation of immune pathways leads to blood-brain barrier disruption, immune cell infiltration, and long-term cognitive impairment.

Summary: This review examines the contribution of innate and adaptive immune cell subsets to POCD pathogenesis. Activated microglia, infiltrating monocytes, and neutrophils initiate neuroinflammatory cascades through cytokine release, while dysregulated T-cell balance (increased Th17 cells, reduced regulatory T cells) exacerbates dysfunction. Key molecular pathways involve damage-associated molecular patterns, complement activation, and impaired neurotrophin signaling. Clinical biomarkers such as IL-6, TNF-α, and S100B show predictive value, with sensitivity of 65-85% and specificity of 75-90%. Current therapeutic strategies include dexmedetomidine, anti-inflammatory agents, and comprehensive perioperative optimization.

Key messages: POCD is a frequent postoperative complication linked to immune dysregulation and neuroinflammation. Both innate and adaptive immune cells play central roles, with microglial polarization and T-cell imbalance as major drivers. Biomarkers such as IL-6, TNF-α, and S100B can support risk stratification and early intervention. Immunomodulatory therapies and perioperative optimization represent promising approaches to reduce POCD incidence and improve patient outcomes.