ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2012
Candesartan, an angiotensin II AT₁-receptor blocker and PPAR-γ agonist, reduces lesion volume and improves motor and memory function after traumatic brain injury in mice.
Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers, 1 of them a synthesis that pooled it.
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Who cites it
73 citing papers in PubMed, 1 synthesis or guideline pooled it, 124 citations in OpenAlex.
- Evidence-based nutritional and pharmacological interventions targeting chronic low-grade inflammation in middle-age and older adults: A systematic review and meta-analysis.Ageing research reviews · 2018Pooled it
- Nose-to-brain delivery of candesartan-loaded nanoemulsion: brain biodistribution and neurobehavioral outcomes in controlled cortical impact-induced traumatic brain injury.Inflammopharmacology · 2026Article
- A Retrospective Analysis of Human Angiotensin II Receptor Blockers (ARB) Pharmacokinetics, Dosages and CBasic & clinical pharmacology & toxicology · 2026Review
- Ang II-mediated effects on BBB integrity in psychiatric and neurological disorders.Progress in neuro-psychopharmacology & biological psychiatry · 2026Review
- Targeting ATScientific reports · 2026Article
- CSF1R and IL1R1 inhibitors synergistically attenuate the early pathogenesis of traumatic brain injury in mice.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Article
- The border-associated macrophage marker MRC1 contributes to an early neuroprotective inflammatory response to traumatic brain injury in mice.Acta neuropathologica communications · 2025Article
- The application of telmisartan in central nervous system disorders.Pharmacological reports : PR · 2025Review
- Sex-specific effects of fecal microbiota transplantation on TBI-exacerbated Alzheimer's pathology in mice.bioRxiv : the preprint server for biology · 2025Article
- Role of the renin-angiotensin pathway in epilepsy: a strategy for its management by drug repurposing.Molecular biology reports · 2025Review
- Inhibiting neddylation: A new strategy for tumor therapy.Journal of pharmaceutical analysis · 2025Review
- Probiotic treatment induces sex-dependent neuroprotection and gut microbiome shifts after traumatic brain injury.Journal of neuroinflammation · 2025Article
- Sex-specific effects of fecal microbiota transplantation on TBI-exacerbated Alzheimer's disease pathology in mice.Frontiers in microbiology · 2025Article
- Sex-dependent improvement in traumatic brain injury outcomes after liposomal delivery of dexamethasone in mice.Bioengineering & translational medicine · 2024Article
- Dual-targeting AAV9P1-mediated neuronal reprogramming in a mouse model of traumatic brain injury.Neural regeneration research · 2024Article
- Neurobehavioral and inflammatory responses following traumatic brain injury in male and female mice.Behavioural brain research · 2024Article
- Reactive gliosis in traumatic brain injury: a comprehensive review.Frontiers in cellular neuroscience · 2024Review
- Inflammatory signaling pathways in the treatment of Alzheimer's disease with inhibitors, natural products and metabolites (Review).International journal of molecular medicine · 2023Review
- The Renin Angiotensin System as a Therapeutic Target in Traumatic Brain Injury.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023Review
- Phosphodiesterase-5 (PDE-5) Inhibitors as Therapy for Cerebrovascular Dysfunction in Chronic Traumatic Brain Injury.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023Review
13 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Traumatic brain injury (TBI) results in complex pathological reactions, the initial lesion worsened by secondary inflammation and edema. Angiotensin II (Ang II) is produced in the brain and Ang II receptor type 1 (AT₁R) overstimulation produces vasoconstriction and inflammation. Ang II receptor blockers (ARBs) are neuroprotective in models of stroke but little is known of their effect when administered in TBI models. We therefore performed controlled cortical impact (CCI) injury on mice to investigate whether the ARB candesartan would mitigate any effects of TBI. We administered candesartan or vehicle to mice 5 h before CCI injury. Candesartan treatment reduced the lesion volume after CCI injury by approximately 50%, decreased the number of dying neurons, lessened the number of activated microglial cells, protected cerebral blood flow (CBF), and reduced the expression of the cytokine TGFβ1 while increasing expression of TGFβ3. Candesartan-treated mice also showed better motor skills on the rotarod 3 days after injury, and improved performance in the Morris water maze 4 weeks after injury. These results indicate that candesartan is neuroprotective, reducing neuronal injury, decreasing lesion volume and microglial activation, protecting CBF and improving functional behavior in a mouse model of TBI. Co-treatment with a peroxisome proliferator-activated receptor-gamma (PPARγ) antagonist significantly reduced some of the beneficial effects of candesartan after CCI, suggesting that PPARγ activation may contribute to part or to all of the neuroprotective effect of candesartan. Overall, our data suggest that ARBs with dual AT₁R-blocking and PPARγ activation properties may have therapeutic value in treating TBI.
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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.