Chronic traumatic encephalopathy: A devastating legacy of repetitive concussion.
Level 5 - mechanism / opinion, no new human data
Narrative review synthesizing mechanistic and clinical literature without systematic review methodology.
PubMed 42341996 · doi:10.1016/j.nbd.2026.107508
What was done
The authors conducted a narrative review synthesizing literature across epidemiology, neuropathology, clinical studies, and experimental platforms (including in vivo systems and 3D in vitro models) to describe the continuum linking repetitive concussive and subconcussive traumatic brain injuries to chronic traumatic encephalopathy (CTE).
What was found
The abstract reports no quantitative measurements, sample sizes, or statistical values. It outlines a disease trajectory wherein primary biomechanical impacts induce secondary cascades (mitochondrial dysfunction, metabolic stress, neuroinflammation, and axonal injury across vascular, glial, and neuronal compartments), promoting protein misfolding of tau, amyloid precursor protein, and TDP-43. It identifies perivascular hyperphosphorylated tau at the depths of cortical sulci as the defining neuropathological feature and notes that existing clinical diagnostic frameworks, fluid biomarkers, and imaging modalities remain limited in diagnostic specificity.
Why it matters
This review integrates diverse biological pathways into a unified continuum from initial physical trauma to localized neurodegeneration, helping direct translational focus toward targeted biomarkers and model development.
Limits
The paper provides no primary empirical data or systematic review metrics. In-life clinical detection remains constrained by non-specific biomarkers, and current laboratory models cannot fully reproduce the complete human disease trajectory.
Cited by
- supports Chronic traumatic encephalopathy (CTE) can continue to progress and worsen even after repetitive head trauma has ceased due to an ongoing feed-forward neuroinflammatory process.