ArticleInternational journal of molecular sciences2021
RETRACTED: Sodium Benzoate, a Metabolite of Cinnamon and a Food Additive, Improves Cognitive Functions in Mice after Controlled Cortical Impact Injury.
Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 14 papers.
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
14 citing papers in PubMed, 18 citations in OpenAlex.
- Sodium benzoate treatment decreased amyloid beta peptides and improved cognitive function among patients with Alzheimer's disease: secondary analysis of a randomized clinical trial.Translational psychiatry · 2025Trial
- Corrected Version: Protection of Mice from Controlled Cortical Impact Injury by Food Additive Glyceryl Tribenzoate.Journal of clinical & experimental immunology · 2026Article
- RETRACTED: Rangasamy et al. Sodium Benzoate, a Metabolite of Cinnamon and a Food Additive, Improves Cognitive Functions in Mice After Controlled Cortical Impact Injury.International journal of molecular sciences · 2026Article
- Parental sodium benzoate diet induces fat accumulation in offspring via histone H3K9me3 and SKN-1/Nrf2.Current research in food science · 2026Article
- Corrected Version: Sodium Benzoate, A Metabolite of Cinnamon and A Food Additive, Improves Cognitive Functions in Mice After Controlled Cortical Impact Injury.Journal of clinical & experimental immunology · 2026Article
- Benzoate Drugs for Traumatic Brain Injury.Journal of clinical & experimental immunology · 2026Article
- Sodium Benzoate Induces Fat Accumulation and Reduces Lifespan via the SKN-1/Nrf2 Signaling Pathway: Evidence from theNutrients · 2024Article
- Protective Effects of Plant-Derived Compounds Against Traumatic Brain Injury.Molecular neurobiology · 2024Review
- Ocrelizumab alters the circulating metabolome in people with relapsing-remitting multiple sclerosis.Annals of clinical and translational neurology · 2024Article
- Therapeutic efficacy of cinnamein, a component of balsam of Tolu/Peru, in controlled cortical impact mouse model of TBI.Neurochemistry international · 2024Article
- Metabolome-Wide Mendelian Randomization Assessing the Causal Role of Serum and Cerebrospinal Metabolites in Traumatic Brain Injury.Biomedicines · 2024Article
- Nebulization of low-dose aspirin ameliorates Huntington's pathology in N171-82Q transgenic mice.NeuroImmune pharmacology and therapeutics · 2024Article
- Amelioration of experimental autoimmune encephalomyelitis by gemfibrozil in mice via PPARβ/δ: implications for multiple sclerosis.Frontiers in cellular neuroscience · 2024Article
- RETRACTED: Protection of Mice from Controlled Cortical Impact Injury by Food Additive Glyceryl Tribenzoate.International journal of molecular sciences · 2023Article
Corrections and comments
- Retracted
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Traumatic brain injury (TBI) is a major health concern, sometimes leading to long-term neurological disability, especially in children, young adults and war veterans. Although research investigators and clinicians have applied different treatment strategies or neurosurgical procedures to solve this health issue, we are still in need of an effective therapy to halt the pathogenesis of brain injury. Earlier, we reported that sodium benzoate (NaB), a metabolite of cinnamon and a Food and Drug Administration-approved drug against urea cycle disorders and glycine encephalopathy, protects neurons in animal models of Parkinson's disease and Alzheimer's disease. This study was undertaken to examine the therapeutic efficacy of NaB in a controlled cortical impact (CCI)-induced preclinical mouse model of TBI. Oral treatment with NaB, but not sodium formate (NaFO), was found to decrease the activation of microglia and astrocytes and to inhibit the expression of inducible nitric oxide synthase (iNOS) in the hippocampus and cortex of CCI-insulted mice. Further, administration of NaB also reduced the vascular damage and decreased the size of the lesion cavity in the brain of CCI-induced mice. Importantly, NaB-treated mice showed significant improvements in memory and locomotor functions as well as displaying a substantial reduction in depression-like behaviors. These results delineate a novel neuroprotective property of NaB, highlighting its possible therapeutic importance in TBI.
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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.