ReviewProgress in neurobiology2017
Chronic traumatic encephalopathy-integration of canonical traumatic brain injury secondary injury mechanisms with tau pathology.
Review in Progress in neurobiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
35 citing papers in PubMed, 67 citations in OpenAlex.
- Article
- Remimazolam Attenuates Neurological Injury After TBI: A Potential Role of α7nAChR-Associated Mitophagy Enhancement and Pyroptosis Suppression in BV2 Cells.Drug design, development and therapy · 2026Article
- Impact Induces Phagocytic Defect in Reactive Microglia.bioRxiv : the preprint server for biology · 2025Article
- Review
- Advances in research on biomaterials and stem cell/exosome-based strategies in the treatment of traumatic brain injury.Acta pharmaceutica Sinica. B · 2025Review
- Translational Outcomes Project in Neurotrauma (TOP-NT) Pre-Clinical Consortium Study: A Synopsis.Journal of neurotrauma · 2025Article
- Traumatic Brain Injury and Chronic Traumatic Encephalopathy: Not Only Trigger for Neurodegeneration but Also for Cerebral Amyloid Angiopathy?Biomedicines · 2025Review
- Early cerebrospinal fluid elevations of pTau-217 in severe traumatic brain injury subjects.Frontiers in neurology · 2025Article
- Metabolic Surgery and Chronic Traumatic Encephalopathy: Perceptions of Former NFL Players.Obesity surgery · 2024Article
- Transcending Traditional Treatment: The Therapeutical Potential of Nanovesicles for Transdermal Baclofen Delivery in Repeated Traumatic Brain Injury.Advanced pharmaceutical bulletin · 2024Article
- Hyperphosphorylated Tau Inflicts Intracellular Stress Responses that Are Mitigated by Apomorphine.Molecular neurobiology · 2024Article
- Knockout ofNeural regeneration research · 2023Article
- Co-administration of Nanowired Oxiracetam and Neprilysin with Monoclonal Antibodies to Amyloid Beta Peptide and p-Tau Thwarted Exacerbation of Brain Pathology in Concussive Head Injury at Hot Environment.Advances in neurobiology · 2023Review
- Utilizing novel TBI-on-a-chip device to link physical impacts to neurodegeneration and decipher primary and secondary injury mechanisms.Scientific reports · 2022Article
- Angiotensin-(1-7) improves cognitive function and reduces inflammation in mice following mild traumatic brain injury.Frontiers in behavioral neuroscience · 2022Article
- PDIA3 inhibits mitochondrial respiratory function in brain endothelial cells and C. elegans through STAT3 signaling and decreases survival after OGD.Cell communication and signaling : CCS · 2021Article
- Modeling links softening of myelin and spectrin scaffolds of axons after a concussion to increased vulnerability to repeated injuries.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Expression of GFAP and Tau Following Blast Exposure in the Cerebral Cortex of Ferrets.Journal of neuropathology and experimental neurology · 2021Article
- Broader Insights into Understanding Tumor Necrosis Factor and Neurodegenerative Disease Pathogenesis Infer New Therapeutic Approaches.Journal of Alzheimer's disease : JAD · 2021Review
- NLRP3 Inflammasome-Dependent Increases in High Mobility Group Box 1 Involved in the Cognitive Dysfunction Caused by Tau-Overexpression.Frontiers in aging neuroscience · 2021Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
In recent years, a new neurodegenerative tauopathy labeled Chronic Traumatic Encephalopathy (CTE), has been identified that is believed to be primarily a sequela of repeated mild traumatic brain injury (TBI), often referred to as concussion, that occurs in athletes participating in contact sports (e.g. boxing, American football, Australian football, rugby, soccer, ice hockey) or in military combatants, especially after blast-induced injuries. Since the identification of CTE, and its neuropathological finding of deposits of hyperphosphorylated tau protein, mechanistic attention has been on lumping the disorder together with various other non-traumatic neurodegenerative tauopathies. Indeed, brains from suspected CTE cases that have come to autopsy have been confirmed to have deposits of hyperphosphorylated tau in locations that make its anatomical distribution distinct for other tauopathies. The fact that these individuals experienced repetitive TBI episodes during their athletic or military careers suggests that the secondary injury mechanisms that have been extensively characterized in acute TBI preclinical models, and in TBI patients, including glutamate excitotoxicity, intracellular calcium overload, mitochondrial dysfunction, free radical-induced oxidative damage and neuroinflammation, may contribute to the brain damage associated with CTE. Thus, the current review begins with an in depth analysis of what is known about the tau protein and its functions and dysfunctions followed by a discussion of the major TBI secondary injury mechanisms, and how the latter have been shown to contribute to tau pathology. The value of this review is that it might lead to improved neuroprotective strategies for either prophylactically attenuating the development of CTE or slowing its progression.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.