Evidence map›Paper›PMID 29569150›Full record

ArticleMetabolic brain disease2018

Impaired lipid metabolism markers to assess the risk of neuroinflammation in autism spectrum disorder.

Hanan Qasem, Laila Al-Ayadhi, Geir Bjørklund, Salvatore Chirumbolo, Afaf El-Ansary

Abstract read
PubMed Publisher
In one paragraph

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.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 15% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.

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  20. 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) · 2020
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 3 institutions in 3 countries.

Hanan QasemBiochemistry Department, Science College, King Saud University, Riyadh, Saudi Arabia.
Laila Al-AyadhiAutism Research and Treatment Center, Riyadh, Saudi Arabia.
Geir BjørklundCouncil for Nutritional and Environmental Medicine, Mo i Rana, Norway.
Salvatore ChirumboloDepartment of Neurological and Movement Sciences, University of Verona, Verona, Italy.
Afaf El-AnsaryAutism Research and Treatment Center, Riyadh, Saudi Arabia. elansary@ksu.edu.sa.
King Saud University · SAThe Research Council of Norway · NOUniversity of Verona · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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

Autism Spectrum DisorderBiomarkersChildChild, PreschoolCognitionCyclooxygenase 2DinoprostoneEncephalitisHumansLipid MetabolismMaleNF-kappa BProstaglandin-E SynthasesSeverity of Illness IndexBiomarkersCyclooxygenase 2DinoprostoneNF-kappa BProstaglandin-E SynthasesPTGES protein, humanAutismChildhood autism rating scaleCyclooxygenase-2, microsomal prostaglandin E synthase-1, neuroinflammationNF-κB: Nuclear factor kappa B, PGE2: prostaglandin E 2, short sensory profileSocial responsiveness scale

Identifiers

PMID29569150
OpenAlexW2792857675

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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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.