ArticleJournal of neuroinflammation2022
Montelukast reduces grey matter abnormalities and functional deficits in a mouse model of inflammation-induced encephalopathy of prematurity.
Article in Journal of neuroinflammation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 20 citations in OpenAlex.
- Montelukast Ameliorates Antimony-Induced Neurotoxicity Accompanied by Alterations in Oxidative Stress, Neuroinflammation, and Mitochondrial Function.Biological trace element research · 2026Article
- Montelukast attenuated memory decline, neuroinflammatory and neurodegenerative biomarkers in AβPsychopharmacology · 2026Article
- Pharmacokinetics, safety and preliminary efficacy study of montelukast in critically ill infants with developing bronchopulmonary dysplasia (PRISM).Contemporary clinical trials communications · 2026Article
- Human chorionic gonadotropin decreases cerebral cystic encephalomalacia and parvalbumin interneuron degeneration in a pro-inflammatory model of mouse neonatal hypoxia-ischemia.Scientific reports · 2026Article
- Cortical mean diffusivity detects early age-related changes and associates with cognition and plasma biomarkers.Brain communications · 2026Article
- Proinflammatory state and metabolic dysregulation linking delayed feeding progression to extrauterine restricted head growth in extremely preterm infants.BMC medicine · 2025Article
- A systematic scoring system to optimise the testing of neurotherapeutics in models of perinatal brain injury, with an applied case study of human umbilical-cord MSC.Journal of neuroinflammation · 2025Article
- Unraveling cysteinyl leukotrienes and their receptors in inflammation through the brain-gut-lung axis.Virulence · 2025Review
- Montelukast alleviates thioacetamide-induced hepatic encephalopathy in rats.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Modulation of Neutrophil Recruitment and Inflammatory Signaling in Acute Respiratory Distress Syndrome by Leukotriene Inhibitors Montelukast and Zileuton.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- New insights on pharmacological potential of montelukast: a comprehensive review.Inflammopharmacology · 2025Review
- The Impact of Montelukast Duration on the Risk of Neuropsychiatric Disorders in Children with Asthma: A Population-Based Cohort Study.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Promising Effects of Montelukast for Critically Ill Asthma Patients via a Reduction in Delirium.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Evaluating the safety and efficacy of the leukotriene receptor antagonist montelukast as adjuvant therapy in obese patients with type 2 diabetes mellitus: A double-blind, randomized, placebo-controlled trial.Frontiers in pharmacology · 2023Article
Corrections and comments
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Authors and funding
17 authors at 3 institutions in 3 countries.
Funding
Abstract
Encephalopathy of prematurity (EoP) affects approximately 30% of infants born < 32 weeks gestation and is highly associated with inflammation in the foetus. Here we evaluated the efficacy of montelukast, a cysteinyl leukotriene receptor antagonist widely used to treat asthma in children, to ameliorate peripheral and central inflammation, and subsequent grey matter neuropathology and behaviour deficits in a mouse model of EoP. Male CD-1 mice were treated with intraperitoneal (i.p.) saline or interleukin-1beta (IL-1β, 40 μg/kg, 5 μL/g body weight) from postnatal day (P)1-5 ± concomitant montelukast (1-30 mg/kg). Saline or montelukast treatment was continued for a further 5 days post-injury. Assessment of systemic and central inflammation and short-term neuropathology was performed from 4 h following treatment through to P10. Behavioural testing, MRI and neuropathological assessments were made on a second cohort of animals from P36 to 54. Montelukast was found to attenuate both peripheral and central inflammation, reducing the expression of pro-inflammatory molecules (IL-1β, IL-6, TNF) in the brain. Inflammation induced a reduction in parvalbumin-positive interneuron density in the cortex, which was normalised with high-dose montelukast. The lowest effective dose, 3 mg/kg, was able to improve anxiety and spatial learning deficits in this model of inflammatory injury, and alterations in cortical mean diffusivity were not present in animals that received this dose of montelukast. Repurposed montelukast administered early after preterm birth may, therefore, improve grey matter development and outcome in EoP.
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Registered trials
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