ArticleJournal of neurotrauma2010
Age-related mitochondrial changes after traumatic brain injury.
Article in Journal of neurotrauma, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 69 citations in OpenAlex.
- Cangfudaotan decoction inhibits mitochondria-dependent apoptosis of granulosa cells in rats with polycystic ovarian syndrome.Frontiers in endocrinology · 2022Trial
- Traumatic brain injury exacerbates mitochondrial dysfunction in APP/PS1 knock-in mice through time-dependent pathways.Experimental neurology · 2026Article
- Cardiac troponin T and 28-day mortality in traumatic brain injury: a retrospective cohort study and machine learning prediction model.Frontiers in neurology · 2026Article
- Traumatic brain injury exacerbates mitochondrial dysfunction in APP/PS1 knock-in mice through time-dependent pathways.bioRxiv : the preprint server for biology · 2025Article
- Article
- Time Course of Mitochondrial Antioxidant Markers in a Preclinical Model of Severe Penetrating Traumatic Brain Injury.International journal of molecular sciences · 2025Article
- Differential CaFrontiers in synaptic neuroscience · 2025Article
- Effect Size of Targeted Temperature Management in Pediatric Patients with Post-Cardiac Arrest Syndrome According to the Severity.Life (Basel, Switzerland) · 2024Article
- Cognition and Behavior in the Aging Brain Following TBI: Surveying the Preclinical Evidence.Advances in neurobiology · 2024Review
- Age at Injury as a Modifier of Preclinical TBI Behavioral, Neuropathological, and Inflammatory Outcomes.Advances in neurobiology · 2024Review
- Mitochondrial Dysfunction After Repeated Mild Blast Traumatic Brain Injury Is Attenuated by a Mild Mitochondrial Uncoupling Prodrug.Journal of neurotrauma · 2023Article
- Fundamental Neurochemistry Review: Microglial immunometabolism in traumatic brain injury.Journal of neurochemistry · 2023Review
- Acute effects of single and repeated mild traumatic brain injury on levels of neurometabolites, lipids, and mitochondrial function in male rats.Frontiers in molecular neuroscience · 2023Article
- Jian-Pi-Yi-Shen decoction inhibits mitochondria-dependent granulosa cell apoptosis in a rat model of POF.Aging · 2022Article
- Renoprotective effect of Tanshinone IIA against kidney injury induced by ischemia-reperfusion in obese rats.Aging · 2022Article
- A possible new activator of PI3K-Huayu Qutan Recipe alleviates mitochondrial apoptosis in obesity rats with acute myocardial infarction.Journal of cellular and molecular medicine · 2022Article
- The killifish visual system as an in vivo model to study brain aging and rejuvenation.NPJ aging and mechanisms of disease · 2021Article
- Tanshinone IIA combined with CsA inhibit myocardial cell apoptosis induced by renal ischemia-reperfusion injury in obese rats.BMC complementary medicine and therapies · 2021Article
- Tanshinone IIA Combined With Cyclosporine A Alleviates Lung Apoptosis Induced by Renal Ischemia-Reperfusion in Obese Rats.Frontiers in medicine · 2021Article
- Protective effects of phenelzine administration on synaptic and non-synaptic cortical mitochondrial function and lipid peroxidation-mediated oxidative damage following TBI in young adult male rats.Experimental neurology · 2020Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Mitochondrial dysfunction is known to occur following traumatic brain injury (TBI) and has been well characterized. This study assessed possible age-related changes in the cortical mitochondrial bioenergetics following TBI. Three hours following a moderate TBI, tissue from the ipsilateral hemisphere (site of impact and penumbra) and the corresponding contralateral region were harvested from young (3- to 5-month-old) and aged (22- to 24-month-old) Fischer 344 rats. Synaptic and extrasynaptic mitochondria were isolated using a Ficoll gradient, and several bioenergetic parameters were examined using a Clark-type electrode. Injury-related respiration deficits were observed in both young and aged rats. Synaptic mitochondria showed an age-related decline in the rate of ATP production, and a decline in respiratory control ratios (RCR), which were not apparent in the extrasynaptic fraction. Following respiration analysis, mitochondrial samples were probed for oxidative damage (3-nitrotyrosine [3-NT], 4-hydroxynonenal [4-HNE], and protein carbonyls [PC]). All markers of oxidative damage were elevated with injury and age in the synaptic fraction, but only with injury in the extrasynaptic fraction. Synaptic mitochondria displayed the highest levels of oxidative damage and may contribute to the synaptic bioenergetic deficits seen following injury. Data indicate that cortical synaptic mitochondria appear to have an increased susceptibility to perturbation with age, suggesting that the increased mitochondrial dysfunction observed following injury may impede recovery in aged animals.
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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.