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Background <p>Chronic traumatic encephalopathy (CTE) is classically defined as a neuroglial tauopathy characterized by perivascular accumulation of hyperphosphorylated tau within neurons and astrocytes. Defining lesions localize to the depths of cortical sulci, implicating vascular and glial elements in early pathogenesis. This systematic scoping review evaluates the extent to which astrocytic dysfunction contributes to CTE pathogenesis, specifically whether astrocytic alterations precede or potentiate neuronal tauopathy.</p> Methods <p>A structured search of PubMed, Embase, Web of Science, and Scopus was conducted from inception through December 2025 in accordance with PRISMA 2020 guidelines. Due to substantial heterogeneity in study design, including postmortem analyses, experimental models, and biomarker studies, a qualitative synthesis was performed.</p> Results <p>Forty studies met inclusion criteria, converging on four domains: (1) interface-specific astrogliosis at perivascular sulcal depths; (2) disruption of aquaporin-4 polarization with uncertain translational relevance in humans; (3) astrocytic degeneration and impaired glutamate homeostasis; and (4) sustained neuroinflammation mediated through astrocyte–microglia signaling. Circulating GFAP emerged as a sensitive but non-specific biomarker of neuroglial injury.</p> Conclusion <p>CTE is best conceptualized as a neuroglial tauopathy in which astrocytes function as integral contributors to disease progression, likely in coordination with microglia. While astrocytic dysfunction may play an early role, its mechanistic specificity relative to other tauopathies remains incompletely defined.</p>

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Astrocytic contributions to the pathogenesis of chronic traumatic encephalopathy: a scoping review

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月21日

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  • Alex Kubiak,
  • Kameron Hahn,
  • Nicholas Powers,
  • Ethan Arroyo,
  • Carson Vandello,
  • Joseph Martins,
  • Ling He

摘要

Background

Chronic traumatic encephalopathy (CTE) is classically defined as a neuroglial tauopathy characterized by perivascular accumulation of hyperphosphorylated tau within neurons and astrocytes. Defining lesions localize to the depths of cortical sulci, implicating vascular and glial elements in early pathogenesis. This systematic scoping review evaluates the extent to which astrocytic dysfunction contributes to CTE pathogenesis, specifically whether astrocytic alterations precede or potentiate neuronal tauopathy.

Methods

A structured search of PubMed, Embase, Web of Science, and Scopus was conducted from inception through December 2025 in accordance with PRISMA 2020 guidelines. Due to substantial heterogeneity in study design, including postmortem analyses, experimental models, and biomarker studies, a qualitative synthesis was performed.

Results

Forty studies met inclusion criteria, converging on four domains: (1) interface-specific astrogliosis at perivascular sulcal depths; (2) disruption of aquaporin-4 polarization with uncertain translational relevance in humans; (3) astrocytic degeneration and impaired glutamate homeostasis; and (4) sustained neuroinflammation mediated through astrocyte–microglia signaling. Circulating GFAP emerged as a sensitive but non-specific biomarker of neuroglial injury.

Conclusion

CTE is best conceptualized as a neuroglial tauopathy in which astrocytes function as integral contributors to disease progression, likely in coordination with microglia. While astrocytic dysfunction may play an early role, its mechanistic specificity relative to other tauopathies remains incompletely defined.