ArticleTranslational psychiatry2021
S100B dysregulation during brain development affects synaptic SHANK protein networks via alteration of zinc homeostasis.
Article in Translational psychiatry, 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, 17 citations in OpenAlex.
- Multiparametric Bioresorbable Sensor for Doxorubicin Detection via Molecularly Imprinted Synthetic Receptors.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Inflammation-induced impairment of synaptic plasticity accelerates atherosclerosis co-depression disease: insights from bioinformatics analysis and transcriptomics.Cell & bioscience · 2026Article
- Hypersynchronous iPSC-derived SHANK2 neuronal networks are rescued by mGluR5 agonism.Stem cell reports · 2025Article
- Development of a Biodegradable Green Emitter Chitosan-Based OLED for Implantable Biomedical Devices.ACS applied materials & interfaces · 2025Article
- In vivo and in situ monitoring of doxorubicin pharmacokinetics with an implantable bioresorbable optical sensor.Science advances · 2025Article
- Secondary Modification of S100B Influences Anti Amyloid-β Aggregation Activity and Alzheimer's Disease Pathology.International journal of molecular sciences · 2024Article
- S100B actions on glial and neuronal cells in the developing brain: an overview.Frontiers in neuroscience · 2024Review
- Article
- SHANK family on stem cell fate and development.Cell death & disease · 2022Review
- Prenatal Zinc Deficient Mice as a Model for Autism Spectrum Disorders.International journal of molecular sciences · 2022Review
- Integration of structural MRI and epigenetic analyses hint at linked cellular defects of the subventricular zone and insular cortex in autism: Findings from a case study.Frontiers in neuroscience · 2022Article
- Brain region and gene dosage-differential transcriptomic changes inFrontiers in molecular neuroscience · 2022Article
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Authors and funding
13 authors at 5 institutions in 6 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autism Spectrum Disorders (ASD) are caused by a combination of genetic predisposition and nongenetic factors. Among the nongenetic factors, maternal immune system activation and zinc deficiency have been proposed. Intriguingly, as a genetic factor, copy-number variations in S100B, a pro-inflammatory damage-associated molecular pattern (DAMP), have been associated with ASD, and increased serum S100B has been found in ASD. Interestingly, it has been shown that increased S100B levels affect zinc homeostasis in vitro. Thus, here, we investigated the influence of increased S100B levels in vitro and in vivo during pregnancy in mice regarding zinc availability, the zinc-sensitive SHANK protein networks associated with ASD, and behavioral outcomes. We observed that S100B affects the synaptic SHANK2 and SHANK3 levels in a zinc-dependent manner, especially early in neuronal development. Animals exposed to high S100B levels in utero similarly show reduced levels of free zinc and SHANK2 in the brain. On the behavioral level, these mice display hyperactivity, increased stereotypic and abnormal social behaviors, and cognitive impairment. Pro-inflammatory factors and zinc-signaling alterations converge on the synaptic level revealing a common pathomechanism that may mechanistically explain a large share of ASD cases.
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