ReviewShock (Augusta, Ga.)2017
The Role of Microglia in the Etiology and Evolution of Chronic Traumatic Encephalopathy.
Review in Shock (Augusta, Ga.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
14 citing papers in PubMed, 24 citations in OpenAlex.
- Short-Chain Fatty Acid Supplementation After Traumatic Brain Injury Attenuates Neurologic Injury Via the Gut-Brain-Microglia Axis.Shock (Augusta, Ga.) · 2026Article
- The evolving pathophysiology of TBI and the advantages of temporally-guided combination therapies.Neurochemistry international · 2024Review
- Traumatic brain injury-associated epigenetic changes and the risk for neurodegenerative diseases.Frontiers in neuroscience · 2023Article
- Differential neuropathology and functional outcome after equivalent traumatic brain injury in aged versus young adult mice.Experimental neurology · 2021Article
- miR-142-3p Expression Is Predictive for Severe Traumatic Brain Injury (TBI) in Trauma Patients.International journal of molecular sciences · 2020Article
- Severe Traumatic Brain Injury (TBI) Modulates the Kinetic Profile of the Inflammatory Response of Markers for Neuronal Damage.Journal of clinical medicine · 2020Article
- Microglia Adopt Longitudinal Transcriptional Changes After Traumatic Brain Injury.The Journal of surgical research · 2020Article
- Microglial Activation and Inflammation as a Factor in the Pathogenesis of Progressive Supranuclear Palsy (PSP).Frontiers in neuroscience · 2020Review
- Murine Model of Controlled Cortical Impact for the Induction of Traumatic Brain Injury.Journal of visualized experiments : JoVE · 2019Article
- Induction of a transmissible tau pathology by traumatic brain injury.Brain : a journal of neurology · 2018Article
- Current understanding of neuroinflammation after traumatic brain injury and cell-based therapeutic opportunities.Chinese journal of traumatology = Zhonghua chuang shang za zhi · 2018Review
- Radiosynthesis and Evaluation of [ACS medicinal chemistry letters · 2018Article
- Article
- Modeling the Long-Term Consequences of Repeated Blast-Induced Mild Traumatic Brain Injuries.Journal of neurotrauma · 2017Article
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 at 1 institution in 1 country.
Funding
Abstract
Chronic traumatic encephalopathy (CTE) is a progressive neurodegenerative disease that presents as a late sequela from traumatic brain injury (TBI). TBI is a growing and under-recognized public health concern with a high degree of morbidity and large associated global costs. While the immune response to TBI is complex, its contribution to the development of CTE remains largely unknown. In this review, we summarize the current understanding of the link between CTE and the resident innate immune system of the brain-microglia. We discuss the neuropathology underlying CTE including the creation and aggregation of phosphorylated tau protein into neurofibrillary tangles and the formation of amyloid beta deposits. We also present how microglia, the resident innate immune cells of the brain, drive the continuous low-level inflammation associated with the insidious onset of CTE. In this review, we conclude that the latency period between the index brain injury and the long-term development of CTE presents an opportunity for therapeutic intervention. Encouraging advances with microtubule stabilizers, cis p-tau antibodies, and the ability to therapeutically alter the inflammatory state of microglia have shown positive results in both animal and human trials. Looking forward, recent advancements in next-generation sequencing technology for the study of genomic, transcriptomic, and epigenetic information will provide an opportunity for significant advancement in our understanding of prorepair and pro-injury gene signatures allowing for targeted intervention in this highly morbid injury process.
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What OpenQuestion holds
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.