ArticleLaboratory investigation; a journal of technical methods and pathology2019
DNA damage as a marker of brain damage in individuals with history of concussions.
Article in Laboratory investigation; a journal of technical methods and pathology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis 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.
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Who cites it
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.
- Cognitive Impairment and Dementia-Related Diagnoses in Chronic Traumatic Encephalopathy: A Systematic Review and Meta-Analysis.Neurology · 2025Pooled it
- The Cause-and-Consequence Relationships between Domestic Abuse and Alzheimer's Disease: Identification of Five Subtypes.Current Alzheimer research · 2026Review
- Cellular senescence and senolytic therapy in traumatic brain injury.Frontiers in neuroscience · 2026Review
- Subcellular functions of tau mediate repair response and synaptic homeostasis in injury.Molecular psychiatry · 2025Article
- Temporal and spatial pattern of DNA damage in neurons following spinal cord Injury in mice.Journal of biomedical science · 2025Article
- Parthanatos drives cognitive decline in repeated brain trauma: MSC-derived exosomes as a novel therapeutic strategy.Frontiers in pharmacology · 2025Article
- Erp57 facilitates ZIKV-induced DNA damage via NS2B/NS3 complex formation.Emerging microbes & infections · 2024Article
- Intricate Role of the Cyclic Guanosine Monophosphate Adenosine Monophosphate Synthase-Stimulator of Interferon Genes (cGAS-STING) Pathway in Traumatic Brain Injury-Generated Neuroinflammation and Neuronal Death.ACS pharmacology & translational science · 2024Review
- Brain pathology and symptoms linked to concussion history: beyond chronic traumatic encephalopathy.Brain communications · 2024Article
- Cellular senescence in brain aging and cognitive decline.Frontiers in aging neuroscience · 2023Review
- The pathological potential of ependymal cells in mild traumatic brain injury.Frontiers in cellular neuroscience · 2023Review
- BRCA1 heterozygosity promotes DNA damage-induced senescence in a sex-specific manner following repeated mild traumatic brain injury.Frontiers in neuroscience · 2023Article
- Article
- Commentary: Type I Interferon Response Is Mediated by NLRX1-cGAS-STING Signaling in Brain Injury.Frontiers in molecular neuroscience · 2022Article
- Early onset senescence and cognitive impairment in a murine model of repeated mTBI.Acta neuropathologica communications · 2021Article
- Cellular Senescence in Traumatic Brain Injury: Evidence and Perspectives.Frontiers in aging neuroscience · 2021Review
- Breast cancer type 1 and neurodegeneration: consequences of deficient DNA repair.Brain communications · 2021Review
- Chronic traumatic encephalopathy neuropathology might not be inexorably progressive or unique to repetitive neurotrauma.Brain : a journal of neurology · 2019Review
- DNA repair deficiency and senescence in concussed professional athletes involved in contact sports.Acta neuropathologica communications · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mild traumatic brain injury (mTBI) is common in many populations, including athletes, veterans, and domestic abuse victims. mTBI can cause chronic symptoms, including depression, irritability, memory problems, and attention deficits. A history of repetitive mTBI has been epidemiologically associated with developing early-onset dementia and neurodegenerative diseases and, in particular, is thought to be the underlying cause of chronic traumatic encephalopathy (CTE)-a progressive tauopathy diagnosed by the presence of perivascular hyperphosphorylated tau protein (p-tau) in the depths of cortical sulci. However, the scarce and focal pathology often seen in CTE does not correlate with the severity of symptoms experienced by patients. This paper proposes accumulation of γH2AX, a marker of double-stranded DNA damage, as a novel pathological marker to identify brain damage post-mTBI. We present two cases of men with history of mTBI. Immunohistochemistry revealed extensive DNA damage throughout the frontal cortex, hippocampus, and brainstem areas. Furthermore, gene expression profiling showed increases of ataxia telangiectasia mutated (ATM) and checkpoint kinase 2 (CHEK2), two serine/threonine kinases recruited in response to double-strand breaks in the DNA damage response pathway. These cases highlight the complex pathophysiology of head trauma, and suggest DNA damage as the molecular mechanism behind mTBI-induced pathology and symptoms.
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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.