ArticleSurgical neurology international2011
Immunoexcitotoxicity as a central mechanism in chronic traumatic encephalopathy-A unifying hypothesis.
Article in Surgical neurology international, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers, 3 of them syntheses that pooled it.
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.
The trial behind it
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
96 citing papers in PubMed, 3 syntheses or guidelines pooled it, 197 citations in OpenAlex.
- Sport-Related Concussion and Mental Health Outcomes in Elite Athletes: A Systematic Review.Sports medicine (Auckland, N.Z.) · 2018Pooled it
- Chronic traumatic encephalopathy in contact sports: a systematic review of all reported pathological cases.PloS one · 2015Pooled it
- Genetic Variants and Persistent Impairment Following Mild Traumatic Brain Injury: A Systematic Review.The Journal of head trauma rehabilitationPooled it
- Male mice are particularly vulnerable to cognitive impairment following mTBI.bioRxiv : the preprint server for biology · 2026Article
- Sex, but not exposure-related variables, predicts baseline serum glial fibrillar acidic protein and neurofilament light levels in contact sport athletes.BMJ open sport & exercise medicine · 2026Article
- The Assessment of Selenium, Aluminum, and Zinc in Children with Autism Spectrum Disorder.Biological trace element research · 2025Article
- Advances and Challenges in Traumatic Brain Injury from a Forensic Perspective.Current neuropharmacology · 2025Review
- Immunoexcitoxicity as the mechanism of CNS damage from COVID-19 "vaccinations".Surgical neurology international · 2025Article
- Immunoexcitoxicity as the possible major pathophysiology behind multiple sclerosis and other autoimmune disorders.Surgical neurology international · 2025Article
- Cannabinoid Therapy in Athletics: A Review of Current Cannabis Research to Evaluate Potential Real-World Cannabinoid Applications in Sport.Sports medicine (Auckland, N.Z.) · 2024Review
- Gene Expression Alterations in Peripheral Blood Following Sport-Related Concussion in a Prospective Cohort of Collegiate Athletes: A Concussion Assessment, Research and Education (CARE) Consortium Study.Sports medicine (Auckland, N.Z.) · 2024Article
- Psychedelics for acquired brain injury: a review of molecular mechanisms and therapeutic potential.Molecular psychiatry · 2024Review
- The effect ofSurgical neurology international · 2024Article
- Additive aluminum as a cause of induced immunoexcitoxicity resulting in neurodevelopmental and neurodegenerative disorders: A biochemical, pathophysiological, and pharmacological analysis.Surgical neurology international · 2024Article
- Blood brain barrier disruption and glutamatergic excitotoxicity in post-acute sequelae of SARS COV-2 infection cognitive impairment: potential biomarkers and a window into pathogenesis.Frontiers in neurology · 2024Article
- Single Versus Repetitive Traumatic Brain Injury: Current Knowledge on the Chronic Outcomes, Neuropathology and the Role of TDP-43 Proteinopathy.Experimental neurobiology · 2023Review
- Mild traumatic brain injury as a pathological process.Heliyon · 2023Review
- A Review of the Most Recent Clinical and Neuropathological Criteria for Chronic Traumatic Encephalopathy.Healthcare (Basel, Switzerland) · 2023Review
- Understanding the Molecular Progression of Chronic Traumatic Encephalopathy in Traumatic Brain Injury, Aging and Neurodegenerative Disease.International journal of molecular sciences · 2023Review
- Pilot study protocol of a randomized controlled trial for the potential effects of creatine monohydrate on persistent post-concussive symptoms.Frontiers in neurology · 2023Article
36 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Some individuals suffering from mild traumatic brain injuries, especially repetitive mild concussions, are thought to develop a slowly progressive encephalopathy characterized by a number of the neuropathological elements shared with various neurodegenerative diseases. A central pathological mechanism explaining the development of progressive neurodegeneration in this subset of individuals has not been elucidated. Yet, a large number of studies indicate that a process called immunoexcitotoxicity may be playing a central role in many neurodegenerative diseases including chronic traumatic encephalopathy (CTE). The term immunoexcitotoxicity was first coined by the lead author to explain the evolving pathological and neurodevelopmental changes in autism and the Gulf War Syndrome, but it can be applied to a number of neurodegenerative disorders. The interaction between immune receptors within the central nervous system (CNS) and excitatory glutamate receptors trigger a series of events, such as extensive reactive oxygen species/reactive nitrogen species generation, accumulation of lipid peroxidation products, and prostaglandin activation, which then leads to dendritic retraction, synaptic injury, damage to microtubules, and mitochondrial suppression. In this paper, we discuss the mechanism of immunoexcitotoxicity and its link to each of the pathophysiological and neurochemical events previously described with CTE, with special emphasis on the observed accumulation of hyperphosphorylated tau.
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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.