ArticleJournal of neurotrauma2019
Carnosic Acid Improves Outcome after Repetitive Mild Traumatic Brain Injury.
Article in Journal of neurotrauma, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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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
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.
- Temporal patterns of microglial activation in white matter following experimental mild traumatic brain injury: a systematic literature review.Acta neuropathologica communications · 2021Pooled it
- Trial
- Mitochondrial-targeted therapies in traumatic brain injury: From bench to bedside.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Review
- Sex-specific antioxidant biomarker depletion in patients with a history of mild traumatic brain injury.Advances in redox research · 2024Article
- Anti-Inflammatory Therapeutic Mechanisms of Natural Products: Insight from Rosemary Diterpenes, Carnosic Acid and Carnosol.Biomedicines · 2023Review
- Potential Therapeutic Use of the Rosemary Diterpene Carnosic Acid for Alzheimer's Disease, Parkinson's Disease, and Long-COVID through NRF2 Activation to Counteract the NLRP3 Inflammasome.Antioxidants (Basel, Switzerland) · 2022Review
- Targeting Nrf2-Mediated Oxidative Stress Response in Traumatic Brain Injury: Therapeutic Perspectives of Phytochemicals.Oxidative medicine and cellular longevity · 2022Review
- Impaired Experience-Dependent Refinement of Place Cells in a Rat Model of Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2022Article
- Rescuing mitochondria in traumatic brain injury and intracerebral hemorrhages - A potential therapeutic approach.Neurochemistry international · 2021Review
- Nrf2 activator PB125® as a carnosic acid-based therapeutic agent against respiratory viral diseases, including COVID-19.Free radical biology & medicine · 2021Review
- Amelioration of oxidative stress and neuroinflammation in lipopolysaccharide-induced memory impairment using Rosmarinic acid in mice.Metabolic brain disease · 2021Article
- The Immune System's Role in the Consequences of Mild Traumatic Brain Injury (Concussion).Frontiers in immunology · 2021Review
- Revisiting Traumatic Brain Injury: From Molecular Mechanisms to Therapeutic Interventions.Biomedicines · 2020Review
- A method for assessing tissue respiration in anatomically defined brain regions.Scientific reports · 2020Article
- Transcriptional activation of antioxidant gene expression by Nrf2 protects against mitochondrial dysfunction and neuronal death associated with acute and chronic neurodegeneration.Experimental neurology · 2020Review
- Tannic Acid Provides Neuroprotective Effects Against Traumatic Brain Injury Through the PGC-1α/Nrf2/HO-1 Pathway.Molecular neurobiology · 2020Article
- Carnosic acid alleviates brain injury through NF‑κB‑regulated inflammation and Caspase‑3‑associated apoptosis in high fat‑induced mouse models.Molecular medicine reports · 2019Article
- Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
In the majority of cases, the cognitive and behavioral impairments resulting from a mild traumatic brain injury (TBI) (also referred to as concussion) wane within days to weeks. In contrast, these impairments can persist for months to years after repetitive mild TBI (rmTBI). The cellular and molecular mechanisms underlying these impairments are not well understood. In the present study, we examined the consequences of rmTBI (three weight drops each separated by 72 h) on brain tissue respiration, pathology, and cognitive performance in mice. The transcription factor nuclear factor-erythroid 2-realted factor 2 (Nrf2) has been demonstrated to enhance the expression of numerous cytoprotective genes. Carnosic acid (CA) has been shown to activate Nrf2 and suppress the proinflammatory transcription factor nuclear factor kappa B (NF-κB). Because contemporaneous activation of cytoprotective genes and inhibition of proinflammatory genes can be beneficial, we questioned whether CA can be used to mitigate the pathobiology of rmTBI. The rmTBI increased hippocampal adenosine triphosphate-linked tissue respiration and proton leak that were unaffected by CA treatment. The rmTBI also caused significant motor and cognitive dysfunction, as tested using the foot fault, Barnes maze, and novel object recognition tasks. These impairments occurred in the absence of visible neuronal or dendritic loss. Post-rmTBI administration of CA significantly improved motor and cognitive function, and decreased Gfap and Iba1 immunoreactivities within white matter tracks. Taken together, these results show that rmTBI can cause cognitive impairments in the absence of overt neuronal pathologies, and post-injury treatment with CA can lessen some of these impairments.
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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.