ReviewInternational journal of molecular sciences2022
Prenatal Zinc Deficient Mice as a Model for Autism Spectrum Disorders.
Review in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 2 of them syntheses that pooled it.
What it found
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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
15 citing papers in PubMed, 2 syntheses or guidelines pooled it, 26 citations in OpenAlex.
- Metal Dyshomeostasis as a Driver of Gut Pathology in Autism Spectrum Disorders.Journal of neurochemistry · 2025Pooled it
- Association between zinc status and autism spectrum disorder in children and adolescents: a systematic review and meta-analysis of case-control studies.Frontiers in nutrition · 2025Pooled it
- Zinc signaling controls astrocyte-dependent synapse modulation via the PAF receptor pathway.Journal of neurochemistry · 2025Article
- The Role of Nutrition, Oxidative Stress, and Trace Elements in the Pathophysiology of Autism Spectrum Disorders.International journal of molecular sciences · 2025Review
- NMDA Receptors in Neurodevelopmental Disorders: Pathophysiology and Disease Models.International journal of molecular sciences · 2024Review
- Characterization of Mice Carrying a Neurodevelopmental Disease-Associated GluN2B(L825V) Variant.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Postnatal zinc deficiency due to giardiasis disrupts hippocampal and cerebellar development.PLoS neglected tropical diseases · 2024Article
- Gestational hypothyroxinemia induces ASD-like phenotypes in behavior, proinflammatory markers, and glutamatergic protein expression in mouse offspring of both sexes.Frontiers in endocrinology · 2024Article
- Zinc Water Prevents Autism-Like Behaviors in the BTBR Mice.Biological trace element research · 2023Article
- Plasma zinc, copper and serum ceruloplasmin levels of autism spectrum disorder children in Bangladesh.Heliyon · 2023Article
- Examining Prenatal Dietary Factors in Association with Child Autism-Related Traits Using a Bayesian Mixture Approach: Results from 2 United States Cohorts.Current developments in nutrition · 2023Article
- A Timm-Nissl multiplane microscopic atlas of rat brain zincergic terminal fields and metal-containing glia.Scientific data · 2023Article
- Metal Profiles in Autism Spectrum Disorders: A Crosstalk between Toxic and Essential Metals.International journal of molecular sciences · 2022Review
- The Role of Zinc and NMDA Receptors in Autism Spectrum Disorders.Pharmaceuticals (Basel, Switzerland) · 2022Review
- Non-Genetic Modifiers of Synaptic Plasticity and Neurotransmission in the Central Nervous System (CNS) in Health and Disease.International journal of molecular sciences · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epidemiological studies have shown a clear association between early life zinc deficiency and Autism Spectrum Disorders (ASD). In line with this, mouse models have revealed prenatal zinc deficiency as a profound risk factor for neurobiological and behavioral abnormalities in the offspring reminiscent of ASD behavior. From these studies, a complex pathology emerges, with alterations in the gastrointestinal and immune system and synaptic signaling in the brain, as a major consequence of prenatal zinc deficiency. The features represent a critical link in a causal chain that leads to various neuronal dysfunctions and behavioral phenotypes observed in prenatal zinc deficient (PZD) mice and probably other mouse models for ASD. Given that the complete phenotype of PZD mice may be key to understanding how non-genetic factors can modify the clinical features and severity of autistic patients and explain the observed heterogeneity, here, we summarize published data on PZD mice. We critically review the emerging evidence that prenatal zinc deficiency is at the core of several environmental risk factors associated with ASD, being mechanistically linked to ASD-associated genetic factors. In addition, we highlight future directions and outstanding questions, including potential symptomatic, disease-modifying, and preventive treatment strategies.
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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.