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September 10, 2025Open Access

From Acute Injury to Chronic Neurodegeneration: Molecular Mechanisms Linking Secondary Brain Injury to Long-Term Pathology

JKJulia K. KaniukNorthwestern University DKDivy KumarNorthwestern University CMChristopher MazurekNorthwestern University

Key Points

Chronic traumatic encephalopathy may develop following traumatic brain injury due to ongoing neuroinflammation.
Emerging biomarkers such as glial fibrillary acidic protein highlight potential diagnostic advancements in TBI.
Integration of neuroimaging and machine learning shows promise for predictive tools in managing TBI outcomes.
Targeting molecular mechanisms remains an uncharted area with potential for new therapeutic development.

Abstract

Traumatic brain injury (TBI) initiates a complex cascade of pathophysiological events that have far-reaching consequences beyond the initial injury. This review examines the current state of the literature on the mechanisms underlying neurotrauma and neuroinflammation, with particular emphasis on the molecular cross-talk between these disparate pathways that ultimately precipitates the development of chronic traumatic encephalopathy (CTE). We integrate this mechanistic knowledge with potential diagnostic biomarkers, such as glial fibrillary acidic protein (GFAP), neurofilament light chain (NfL), and ubiquitin carboxy-terminal hydrolase L1 (UCH-L1), and advances in neuroimaging and machine learning-based predictive tools. Finally, we discuss the current therapeutic approaches under investigation, and highlight which molecular targets have yet to be explored for potential therapeutic development.

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