Exploring potential biomarkers and signaling pathways in neuroinflammation post-traumatic brain injury: insights for synthetic compound-based interventions.

Purpose of the review: Traumatic brain injury (TBI) is a major reason for mortality and long-term neurologic disability worldwide, primarily resulting from road accidents, falls, and sports injuries. This review focuses on the potential biomarkers and signaling pathways involved in neuroinflammation, post-traumatic brain injury and synthetic compound-based treatment approaches.

Recent findings: Neuroinflammation is a critical component of TBI pathology, initiated by the activation of microglia and astrocytes, release of pro-inflammatory mediators, and permeation of peripheral immune cells. While inflammation is essential for debris clearance and tissue repair, excessive or chronic inflammation exacerbates neuronal damage, impairs neurogenesis, and hinders functional recovery. This dual role of neuroinflammation highlights the targeted therapeutic strategies to modulate the inflammatory response. Anti-inflammatory cytokines work to limit inflammation, while pro-inflammatory cytokines and small-molecule drugs reduce inflammation through glucocorticoid receptor activation. Emerging therapeutic approaches focus on attenuating pathologic inflammation while preserving its reparative functions. Pharmacologic agents, such as corticosteroids, nonsteroidal anti-inflammatory drugs (NSAIDs), and experimental compounds targeting specific cytokines or signaling pathways, show promise in preclinical studies. Despite encouraging preclinical results, clinical studies have produced mixed outcomes, highlighting the need for further research. This review explores the molecular mechanisms underlying neuroinflammation in TBI, evaluates current and emerging therapeutic strategies, and discusses the challenges of translating these approaches into clinical practice. To improve prognosis for individuals with TBI and create effective treatments, it is crucial to comprehend the intricate interactions between neuroinflammation and TBI pathophysiology.