ArticleFrontiers in psychology2021
A Translational Perspective of Maternal Immune Activation by SARS-CoV-2 on the Potential Prenatal Origin of Neurodevelopmental Disorders: The Role of the Cholinergic Anti-inflammatory Pathway.
Article in Frontiers in psychology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 22 citations in OpenAlex.
- Impact of maternal stress and COVID-19 exposure during pregnancy on offspring neurodevelopment: signature cohort 12 month follow-up.European child & adolescent psychiatry · 2026Article
- Nauclea officinalis extract rescues working memory deficits in adolescent maternal immune activation offspring by restoring cholinergic signaling.Frontiers in cell and developmental biology · 2026Article
- Cranial ultrasonographic findings in newborns exposed to SARS-CoV-2: a single-centre cross-sectional analysis.Italian journal of pediatrics · 2024Article
- Advancing insights into virus-induced neurodevelopmental disorders through human brain organoid modelling.Expert reviews in molecular medicine · 2024Review
- Viral infections in pregnancy and impact on offspring neurodevelopment: mechanisms and lessons learned.Pediatric research · 2024Review
- Maternal and neonatal outcomes during COVID-19 pandemic and pre-pandemic in an urban slum in North India - A community-based ambispective cohort study.Journal of family medicine and primary care · 2024Article
- Risk of Global Developmental Delay in Infants Born from Mothers with COVID-19: A Cross-Sectional Study.International journal of women's health · 2023Article
- At the crux of maternal immune activation: Viruses, microglia, microbes, and IL-17A.Immunological reviews · 2022Review
- Inflammatory reflex disruption in COVID-19.Clinical & experimental neuroimmunology · 2022Review
- Differential effects of early or late exposure to prenatal maternal immune activation on mouse embryonic neurodevelopment.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Virus-Induced Maternal Immune Activation as an Environmental Factor in the Etiology of Autism and Schizophrenia.Frontiers in neuroscience · 2022Review
- Clinical characterization of dysautonomia in long COVID-19 patients.Scientific reports · 2021Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The emergent Coronavirus Disease 2019 (COVID-19) caused by the Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) could produce a maternal immune activation (MIA) via the inflammatory response during gestation that may impair fetal neurodevelopment and lead to postnatal and adulthood mental illness and behavioral dysfunctions. However, so far, limited evidence exists regarding long-term physiological, immunological, and neurodevelopmental modifications produced by the SARS-CoV-2 in the human maternal-fetal binomial and, particularly, in the offspring. Relevant findings derived from epidemiological and preclinical models show that a MIA is indeed linked to an increased risk of neurodevelopmental disorders in the offspring. We hypothesize that a gestational infection triggered by SARS-CoV-2 increases the risks leading to neurodevelopmental disorders of the newborn, which can affect childhood and the long-term quality of life. In particular, disruption of either the maternal or the fetal cholinergic anti-inflammatory pathway (CAP) could cause or exacerbate the severity of COVID-19 in the maternal-fetal binomial. From a translational perspective, in this paper, we discuss the possible manifestation of a MIA by SARS-CoV-2 and the subsequent neurodevelopmental disorders considering the role of the fetal-maternal cytokine cross-talk and the CAP. Specifically, we highlight the urgent need of preclinical studies as well as multicenter and international databanks of maternal-fetal psychophysiological data obtained pre-, during, and post-infection by SARS-CoV-2 from pregnant women and their offspring.
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