Evidence map›Paper›PMID 24621061›Full record

ReviewNutritional neuroscience2015

Environment, dysbiosis, immunity and sex-specific susceptibility: a translational hypothesis for regressive autism pathogenesis.

Alessandra Mezzelani, Martina Landini, Francesco Facchiano, Maria Elisabetta Raggi, Laura Villa, Massimo Molteni, Barbara De Santis, Carlo Brera, Anna Maria Caroli, Luciano Milanesi and 1 more

Open access · bronzeAbstract readReview
In one paragraph

Review in Nutritional neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
3.3field-weighted citation impact, top 8% 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

33 citing papers in PubMed, 1 synthesis or guideline pooled it, 70 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Bimodal distribution of intestinalGut microbes reports · 2024
    Article
  4. Article
  5. Review
  6. Article
  7. Effects of COVID-19 on children with autism.World journal of virology · 2022
    Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
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  17. Review
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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

11 authors at 5 institutions in 2 countries.

Alessandra Mezzelani
Martina Landini
Francesco Facchiano
Maria Elisabetta Raggi
Laura Villa
Massimo Molteni
Barbara De Santis
Carlo Brera
Anna Maria Caroli
Luciano Milanesi
Anna Marabotti
IRCCS Eugenio Medea · ITIstituto Superiore di Sanità · ITNational Academies of Sciences, Engineering, and Medicine · USInstitute of Biomedical Technologies · ITUniversity of Brescia · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAutism is an increasing neurodevelopmental disease that appears by 3 years of age, has genetic and/or environmental etiology, and often shows comorbid situations, such as gastrointestinal (GI) disorders. Autism has also a striking sex-bias, not fully genetically explainable.

objectiveOur goal was to explain how and in which predisposing conditions some compounds can impair neurodevelopment, why this occurs in the first years of age, and, primarily, why more in males than females.

methodsWe reviewed articles regarding the genetic and environmental etiology of autism and toxins effects on animal models selected from PubMed and databases about autism and toxicology. DISCUSSION: Our hypothesis proposes that in the first year of life, the decreasing of maternal immune protection and child immune-system immaturity create an immune vulnerability to infection diseases that, especially if treated with antibiotics, could facilitate dysbiosis and GI disorders. This condition triggers a vicious circle between immune system impairment and increasing dysbiosis that leads to leaky gut and neurochemical compounds and/or neurotoxic xenobiotics production and absorption. This alteration affects the 'gut-brain axis' communication that connects gut with central nervous system via immune system. Thus, metabolic pathways impaired in autistic children can be affected by genetic alterations or by environment-xenobiotics interference. In addition, in animal models many xenobiotics exert their neurotoxicity in a sex-dependent manner.

conclusionsWe integrate fragmented and multi-disciplinary information in a unique hypothesis and first disclose a possible environmental origin for the imbalance of male:female distribution of autism, reinforcing the idea that exogenous factors are related to the recent rise of this disease.

Indexed as

EnvironmentAnimalsAutistic DisorderBrainChildChild, PreschoolDysbiosisFemaleHumansInfantIntestinesMaleRisk FactorsSex FactorsXenobioticsXenobioticsEnvironmental autismGut dysbiosisImmune systemSex biasXenobiotics

Identifiers

PMID24621061
PMCPMC4485698
OpenAlexW1970304160

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.