Evidence map›Paper›PMID 32720073›Full record

ArticleMolecular neurobiology2020

Maternal Immune Activation Causes Schizophrenia-like Behaviors in the Offspring through Activation of Immune-Inflammatory, Oxidative and Apoptotic Pathways, and Lowered Antioxidant Defenses and Neuroprotection.

Pinku Mani Talukdar, Fazal Abdul, Michael Maes, V S Binu, Ganesan Venkatasubramanian, Bindu M Kutty, Monojit Debnath

Abstract read
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In one paragraph

Article in Molecular neurobiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
3.3field-weighted citation impact, top 6% 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

36 citing papers in PubMed, 72 citations in OpenAlex.

  1. Gut microbiota: contributing to high CVD prevalence in people living with schizophrenia?European archives of psychiatry and clinical neuroscience · 2026
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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

7 authors at 2 institutions in 4 countries.

Pinku Mani TalukdarDepartment of Human Genetics, National Institute of Mental Health and Neurosciences (NIMHANS), Hosur Road, Bangalore, 560029, India.
Fazal AbdulDepartment of Human Genetics, National Institute of Mental Health and Neurosciences (NIMHANS), Hosur Road, Bangalore, 560029, India.
Michael MaesDepartment of Psychiatry, Faculty of Medicine, King Chulalongkorn Memorial Hospital, Bangkok, Thailand.
V S BinuDepartment of Biostatistics, National Institute of Mental Health and Neurosciences (NIMHANS), Bengaluru, India.
Ganesan VenkatasubramanianDepartment of Psychiatry, National Institute of Mental Health and Neurosciences (NIMHANS), Bengaluru, India.
Bindu M KuttyDepartment of Neurophysiology, National Institute of Mental Health and Neurosciences (NIMHANS), Bengaluru, India.
Monojit DebnathDepartment of Human Genetics, National Institute of Mental Health and Neurosciences (NIMHANS), Hosur Road, Bangalore, 560029, India. monozeet@gmail.com.ORCID http://orcid.org/0000-0002-5843-072X
National Institute of Mental Health and Neurosciences · INDeakin University · AU

Funding

Department of Science and Technology, Government of Kerala SR/WOS-A/LS-1219/2014(G)
6 · The paper itself

Abstract

Schizophrenia is a complex neuropsychiatric disorder, influenced by a combined action of genes and environmental factors. The neurodevelopmental origin is one of the most widely recognized etiological models of this heterogeneous disorder. Environmental factors, especially infections during gestation, appear to be a major risk determinant of neurodevelopmental basis of schizophrenia. Prenatal infection may cause maternal immune activation (MIA) and enhance risk of schizophrenia in the offspring. However, the precise mechanistic basis through which MIA causes long-lasting schizophrenia-like behavioral deficits in offspring remains inadequately understood. Herein, we aimed to delineate whether prenatal infection-induced MIA causes schizophrenia-like behaviors through its long-lasting effects on immune-inflammatory and apoptotic pathways, oxidative stress toxicity, and antioxidant defenses in the brain of offspring. Sprague-Dawley rats were divided into three groups (n = 15/group) and were injected with poly (I:C), LPS, and saline at gestational day (GD)-12. Except IL-1β, plasma levels of IL-6, TNF-α, and IL-17A assessed after 24 h were significantly elevated in both the poly (I:C)- and LPS-treated pregnant rats, indicating MIA. The rats born to dams treated with poly (I:C) and LPS displayed increased anxiety-like behaviors and significant deficits in social behaviors. Furthermore, the hippocampus of the offspring rats of both the poly (I:C)- and LPS-treated groups showed increased signs of lipid peroxidation, diminished total antioxidant content, and differentially upregulated expression of inflammatory (TNFα, IL6, and IL1β), and apoptotic (Bax, Cas3, and Cas9) genes but decreased expression of neuroprotective (BDNF and Bcl2) genes. The results suggest long-standing effects of prenatal infections on schizophrenia-like behavioral deficits, which are mediated by immune-inflammatory and apoptotic pathways, increased oxidative stress toxicity, and lowered antioxidant and neuroprotective defenses. The findings suggest that prenatal infections may underpin neurodevelopmental aberrations and neuroprogression and subsequently schizophrenia-like symptoms.

Indexed as

ApoptosisNeuroprotectionOxidative StressSignal TransductionAnimalsAntioxidantsAnxietyBehavior, AnimalBrainFemaleGene Expression RegulationInflammationLipopolysaccharidesPoly I-CPregnancyPrenatal Exposure Delayed EffectsAntioxidantsLipopolysaccharidesPoly I-CThiobarbituric Acid Reactive SubstancesInflammationMaternal immune activationNeuro-immuneNeuroprotectionOxidative stressSchizophrenia-like behaviors

Identifiers

PMID32720073
OpenAlexW3044253833

What OpenQuestion holds

Textmetadata
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.