ReviewTranslational neurodegeneration2017
Pathological correlations between traumatic brain injury and chronic neurodegenerative diseases.
Review in Translational neurodegeneration, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 2 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
67 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Hypoxia and Alpha-Synuclein: Inextricable Link Underlying the Pathologic Progression of Parkinson's Disease.Frontiers in aging neuroscience · 2022Pooled it
- Toward a global and reproducible science for brain imaging in neurotrauma: the ENIGMA adult moderate/severe traumatic brain injury working group.Brain imaging and behavior · 2021Pooled it
- The Dual Roles of Extracellular Vesicle Subtypes in Regulating Traumatic Brain Injury.International journal of molecular sciences · 2026Review
- Concussive injuries induce neuronal stress-dependent tau mislocalization to dendritic spines with acrolein and functional network alteration in TBI-on-a-chip.Lab on a chip · 2025Article
- Quantification of Protein Secondary Structures from Discrete Frequency Infrared Images Using Machine Learning.Applied spectroscopy · 2025Article
- Ligustilide Ameliorates Traumatic Brain Injury in Aged Mice by Attenuating Microglia-Mediated Neuroinflammation.Neurochemical research · 2025Article
- Detection of NLRP3, ASC, and Caspase-1 in serum and cerebrospinal fluid of traumatic brain injury patients: implications for short-term prognosis.Acta neurologica Belgica · 2025Article
- Exploring Molecular Pathways in Exercise-Induced Recovery from Traumatic Brain Injury.Medical science monitor : international medical journal of experimental and clinical research · 2025Review
- Temporal differential effects of post-injury alcohol consumption in a mouse model of blast-induced traumatic brain injury.Neuroscience · 2024Article
- Characterization of Novel SARM1 Inhibitors for the Treatment of Chemotherapy-Induced Peripheral Neuropathy.Biomedicines · 2024Article
- Review of the Brain's Behaviour after Injury and Disease for Its Application in an Agent-Based Model (ABM).Biomimetics (Basel, Switzerland) · 2024Review
- Article
- Injectable Bombyx mori (B. mori) silk fibroin/MXene conductive hydrogel for electrically stimulating neural stem cells into neurons for treating brain damage.Journal of nanobiotechnology · 2024Article
- The contribution of β-amyloid, Tau and α-synuclein to blood-brain barrier damage in neurodegenerative disorders.Acta neuropathologica · 2024Review
- Mapping knowledge of the stem cell in traumatic brain injury: a bibliometric and visualized analysis.Frontiers in neurology · 2024Article
- Associations between concussion and more severe TBIs, mild cognitive impairment, and early-onset dementia among military retirees over 40 years.Frontiers in neurology · 2024Article
- Experimental traumatic brain injury increases epichaperome formation.Neurobiology of disease · 2023Article
- Flexible, Miniaturized Sensing Probes Inspired by Biofuel Cells for Monitoring Synaptically Released Glutamate in the Mouse Brain.Angewandte Chemie (International ed. in English) · 2023Article
- Article
- Stress-Induced Auto-Cannibalism in Patients With a History of Moderate Traumatic Brain Injury.Cureus · 2023Article
7 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
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Traumatic brain injury is among the most common causes of death and disability in youth and young adults. In addition to the acute risk of morbidity with moderate to severe injuries, traumatic brain injury is associated with a number of chronic neurological and neuropsychiatric sequelae including neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease. However, despite the high incidence of traumatic brain injuries and the established clinical correlation with neurodegeneration, the causative factors linking these processes have not yet been fully elucidated. Apart from removal from activity, few, if any prophylactic treatments against post-traumatic brain injury neurodegeneration exist. Therefore, it is imperative to understand the pathophysiological mechanisms of traumatic brain injury and neurodegeneration in order to identify potential factors that initiate neurodegenerative processes. Oxidative stress, neuroinflammation, and glutamatergic excitotoxicity have previously been implicated in both secondary brain injury and neurodegeneration. In particular, reactive oxygen species appear to be key in mediating molecular insult in neuroinflammation and excitotoxicity. As such, it is likely that post injury oxidative stress is a key mechanism which links traumatic brain injury to increased risk of neurodegeneration. Consequently, reactive oxygen species and their subsequent byproducts may serve as novel fluid markers for identification and monitoring of cellular damage. Furthermore, these reactive species may further serve as a suitable therapeutic target to reduce the risk of post-injury neurodegeneration and provide long term quality of life improvements for those suffering from traumatic brain injury.
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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.