ArticleJournal of neuropathology and experimental neurology2022
Tau Pathology in Chronic Traumatic Encephalopathy is Primarily Neuronal.
Article in Journal of neuropathology and experimental neurology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 48 citations in OpenAlex.
- Cortical subpial aging-related tau astrogliopathy in older adult men who participated in youth amateur American-style football.Journal of neuropathology and experimental neurology · 2026Article
- CTE has multiple pathologic variants that might relate to different clinical symptom presentation.Acta neuropathologica · 2026Article
- Astrocytic contributions to the pathogenesis of chronic traumatic encephalopathy: a scoping review.Chinese neurosurgical journal · 2026Review
- Widespread hnRNP K Mislocalisation Suggests Differential Neuronal Vulnerability in the Neurodegenerative and Ageing Human Brain.Neuropathology and applied neurobiology · 2026Article
- Tau catalyzes amyloid-β aggregation and toxicity in a polymorph-dependent manner.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Duration of contact sports play associated with aberrant DNA methylation in human frontal cortex.Research square · 2026Article
- Long intervals between repetitive concussions reduce risk of cognitive impairment and limit microglial activation, astrogliosis, and tauopathy in adolescent rats.Scientific reports · 2025Article
- Article
- Age-informed, attention-based weakly supervised learning for neuropathological image assessment.Brain informatics · 2025Article
- Comparison of multiple quantitative strategies for neuropathologic image analyses.Journal of neuropathology and experimental neurology · 2025Article
- Cortical circuit principles predict patterns of trauma induced tauopathy in humans.Cerebral cortex (New York, N.Y. : 1991) · 2025Article
- Traumatic brain injury or head impacts from contact sports are associated with tau astrogliopathy.Brain : a journal of neurology · 2025Article
- Cellular and molecular mechanisms of pathological tau phosphorylation in traumatic brain injury: implications for chronic traumatic encephalopathy.Molecular neurodegeneration · 2025Review
- Perivascular glial reactivity is a feature of phosphorylated tau lesions in chronic traumatic encephalopathy.Acta neuropathologica · 2025Article
- Sulcal morphology in former American football players.Brain communications · 2025Article
- Neurodegeneration in the cortical sulcus is a feature of chronic traumatic encephalopathy and associated with repetitive head impacts.Acta neuropathologica · 2024Article
- Grey matter ageing-related tau astrogliopathy: associations with brain pathologies and cognitive decline.Brain : a journal of neurology · 2024Article
- Chronic traumatic encephalopathy pathognomonic lesions occurring in isolation adjacent to infiltrative and non-infiltrative white matter lesions.Journal of neuropathology and experimental neurology · 2024Article
- Limbic-predominant age-related TDP-43 encephalopathy (LATE-NC): Co-pathologies and genetic risk factors provide clues about pathogenesis.Journal of neuropathology and experimental neurology · 2024Review
- Overexpression of pathogenic tau in astrocytes causes a reduction in AQP4 and GLT1, an immunosuppressed phenotype and unique transcriptional responses to repetitive mild TBI without appreciable changes in tauopathy.Journal of neuroinflammation · 2024Article
Corrections and comments
- Erratum issued
Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Millions of individuals are exposed to repetitive head impacts (RHI) each year through contact sports, military blast, and interpersonal violence. RHI is the major risk factor for developing chronic traumatic encephalopathy (CTE), a neurodegenerative tauopathy. Recent consensus criteria defined the pathognomonic lesion in CTE as perivascular, hyperphosphorylated tau (p-tau) in neuronal aggregates. Astroglial p-tau is an inconsistent supporting feature and not in itself diagnostic of CTE. This study quantitated the spatial and cellular distribution of p-tau pathology in postmortem dorsolateral frontal cortex of 150 individuals with CTE, from ages 21 to 80 years old, without comorbid pathology. p-Tau-immunoreactive cells were quantitated in the gray matter sulcus, crest, subpial region, and within pathognomonic CTE lesions. Significantly more neuronal p-tau than astrocytic p-tau was found across all cortical regions (p < 0.0001). Sulcal astrocytic p-tau was primarily (75%, p < 0.0001) localized to subpial regions as thorn-shaped astrocytes, a form of age-related tau astrogliopathy. Neuronal p-tau was significantly associated with age, years of RHI exposure, and CTE severity; astrocytic p-tau pathology was only significantly associated with age. These findings strongly support neuronal degeneration as a driving feature of CTE and will help inform future research and the development of fluid biomarkers for the detection of neuronal degeneration in CTE.
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