ArticleMetabolic brain disease2018
Impaired lipid metabolism markers to assess the risk of neuroinflammation in autism spectrum disorder.
Article in Metabolic brain disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
26 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.
- Bibliometric study of neuroinflammation in autism spectrum disorder.Frontiers in psychiatry · 2023Pooled it
- Serum TLR4, NF-κB, and NLRP3 Levels in Children with Attention-Deficit/Hyperactivity Disorder: A Case-Control Study.Children (Basel, Switzerland) · 2026Article
- Environmental metals, prostaglandin pathways, and immune-mediated neuroinflammation in autism spectrum disorder: A secondary analysis of peripheral biomarker studies.Metabolic brain disease · 2026Article
- Article
- Association of Clinical Severity in Autism Spectrum Disorder with Biomolecules Involved in Lipid Metabolism, Inflammation and miRNAs.Biomolecules · 2026Article
- Microbiota-gut-brain axis and neuroendocrine pathways underlie divergent mechanisms of intermittent and continuous theta-burst stimulation in autism spectrum disorder.Cellular and molecular life sciences : CMLS · 2026Article
- Interplay Between VCAM-1 and PGE2 Levels and Autism Spectrum Disorder Severity in Children-A Preliminary Single-Center Analysis.Children (Basel, Switzerland) · 2025Article
- Genetic and Environmental Risk Factors for Autism Spectrum Disorder in Saudi Arabia: A Systematic Review.Cureus · 2025Review
- Prostaglandins: Biological Action, Therapeutic Aspects, and Pathophysiology of Autism Spectrum Disorders.Current issues in molecular biology · 2025Review
- Comparison of HMGB1, RAGE, TLR4, and NF-κB levels in children and adolescents diagnosed with autism spectrum disorder with healthy controls.International journal of developmental disabilities · 2025Article
- Untargeted urine metabolomics and machine learning provide potential metabolic signatures in children with autism spectrum disorder.Frontiers in psychiatry · 2024Article
- Microbiota-indole 3-propionic acid-brain axis mediates abnormal synaptic pruning of hippocampal microglia and susceptibility to ASD in IUGR offspring.Microbiome · 2023Article
- Neuroinflammation, Energy and Sphingolipid Metabolism Biomarkers Are Revealed by Metabolic Modeling of Autistic Brains.Biomedicines · 2023Article
- Altered Metabolic Characteristics in Plasma of Young Boys with Autism Spectrum Disorder.Journal of autism and developmental disorders · 2022Article
- Prostanoid Metabolites as Biomarkers in Human Disease.Metabolites · 2022Review
- Article
- Influence of the Aryl Hydrocarbon Receptor Activating Environmental Pollutants on Autism Spectrum Disorder.International journal of molecular sciences · 2021Review
- Perturbed MAPK signaling in ASD: Impact of metal neurotoxicity.Current opinion in toxicology · 2021Article
- The Role of Cholesterol and Fatty Acids in the Etiology and Diagnosis of Autism Spectrum Disorders.International journal of molecular sciences · 2021Review
- Environmental influence on neurodevelopmental disorders: Potential association of heavy metal exposure and autism.Journal of trace elements in medicine and biology : organ of the Society for Minerals and Trace Elements (GMS) · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autism spectrum disorder (ASD) is a multifactorial disorder caused by an interaction between environmental risk factors and a genetic background. It is characterized by impairment in communication, social interaction, repetitive behavior, and sensory processing. The etiology of ASD is still not fully understood, and the role of neuroinflammation in autism behaviors needs to be further investigated. The aim of the present study was to test the possible association between prostaglandin E2 (PGE2), cyclooxygenase-2 (COX-2), microsomal prostaglandin E synthase-1 (mPGES-1), prostaglandin PGE2 EP2 receptors and nuclear kappa B (NF-κB) and the severity of cognitive disorders, social impairment, and sensory dysfunction. PGE2, COX-2, mPGES-1, PGE2-EP2 receptors and NF-κB as biochemical parameters related to neuroinflammation were determined in the plasma of 47 Saudi male patients with ASD, categorized as mild to moderate and severe as indicated by the Childhood Autism Rating Scale (CARS) or the Social Responsiveness Scale (SRS) or the Short Sensory Profile (SSP) and compared to 46 neurotypical controls. The data indicated that ASD patients have remarkably higher levels of the measured parameters compared to neurotypical controls, except for EP2 receptors that showed an opposite trend. While the measured parameter did not correlate with the severity of social and cognitive dysfunction, PGE2, COX-2, and mPGES-1 were remarkably associated with the dysfunction in sensory processing. NF-κB was significantly increased in relation to age. Based on the discussed data, the positive correlation between PGE2, COX-2, and mPGES-1 confirm the role of PGE2 pathway and neuroinflammation in the etiology of ASD, and the possibility of using PGE2, COX-2 and mPGES-1 as biomarkers of autism severity. NF-κB as inflammatory inducer showed an elevated level in plasma of ASD individuals. Receiver operating characteristic analysis together with predictiveness diagrams proved that the measured parameters could be used as predictive biomarkers of biochemical correlates to ASD.
Indexed as
Identifiers
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.