Neuroinflammatory mechanisms may help identify candidate biomarkers in chronic traumatic encephalopathy (CTE)

TL;DR

This paper explores how neuroinflammation could help identify new biomarkers for diagnosing chronic traumatic encephalopathy (CTE), a brain disease linked to repeated head injuries.

Contribution

The paper proposes that neuroinflammatory markers like CCL11, CCL21, and GFAP could serve as novel, specific biomarkers for CTE.

Findings

Neuroinflammation is a key part of early CTE development and may act as a disease-specific marker.

Immune mediators such as CCL11, CCL21, and GFAP show potential as diagnostic biomarkers for CTE.

Further research is needed to validate these immune markers for clinical use in CTE diagnosis.

Abstract

Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease that can
only be diagnosed post-mortem via pathological autopsy. The primary risk factor
for CTE is a history of repetitive head impacts (RHI) received through contact
sports including American football, hockey or soccer, military-related head
injuries, or intimate partner violence. Recent findings have demonstrated that
neuroinflammation is a critical compo-nent of early CTE pathogenesis and is
likely part of the mechanism driving disease onset and progression.
Additionally, the innate specificity, or ‘signature’, of a neuroinflammatory
response may function as a dis-ease-specific marker for various
neurodegenerative conditions. This would suggest an enormous repository of novel
CTE biomarker candidates to be added to ongoing clinical trials, helping bolster
diagnosis. However, few studies have truly leveraged immune mediators as
candidate CTE markers. In this review, we argue and provide support that
inflammatory mechanisms could serve as a viable source for novel biomarkers that
are specific to CTE pathol-ogy. This includes an evaluation of inflammatory or
damage-related markers such as CCL11 (C-C Motif Chem-okine Ligand 11, also known
as Eotaxin-1), CCL21 (C-C Motif Chemokine Ligand 21) and GFAP (Glial Fibrillary
Acidic Protein). We discuss the neuroinflammatory responses that give rise to
these biomarkers in addition to the advantages and limitations of using each to
diagnose CTE with particular attention to sensitivity and specifici-ty. Although
further research is necessary to validate immune mediators, the latter show
promise as diagnos-tic biomarkers for CTE and may also eventually serve as
therapeutic targets for mitigating chronic inflamma-tion in at-risk
populations.

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