ArticleFrontiers in molecular neuroscience2023
Intermittent hypoxia-induced enhancement of sociability and working memory associates with CNTNAP2 upregulation.
Article in Frontiers in molecular neuroscience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 4 citations in OpenAlex.
- Histone H1 variants regulate neurodevelopmental transcriptional programs in autism with 16p11.2 deletion.Genome biology · 2026Article
- Aerobic exercise training improves learning and memory performance in hypoxic-exposed rats by activating the hippocampal PKA-CREB-BDNF signaling pathway.BMC neuroscience · 2025Article
- Future Therapeutic Strategies for Alzheimer's Disease: Focus on Behavioral and Psychological Symptoms.International journal of molecular sciences · 2024Review
- Contactin-associated protein-like 2 (CNTNAP2) mutations impair the essential α-secretase cleavages, leading to autism-like phenotypes.Signal transduction and targeted therapy · 2024Article
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Hypoxia is an environmental risk factor for many disorders throughout life. Perinatal hypoxia contributes to autism spectrum disorder (ASD), while hypoxic conditions in the elderly facilitate memory deficits. However, the effects of hypoxia on adolescence remains elusive. CNTNAP2 is a critical molecule in ASD pathogenesis with undefined mechanisms. We investigate hypoxia's impact on adolescence and the underlying mechanism related to CNTNAP2. Methods: Three-chamber social approach test, Y maze, Morris Water Maze and Open Field Test were applied to evaluate behavioral alterations. Immunoblotting, 5'- RACE and dual-luciferase reporter assay were performed to examine CNTNAP2 protein expression, transcription start site (TSS) of human CNTNAP2 gene and CNTNAP2 promoter activity, respectively. Results: Intermittent hypoxia treatment improved social behaviors and working memory in adolescent mice. CNTNAP2 was increased in the brains of hypoxia-treated mice. The sequencing results identified the TSS at 518 bp upstream of the translation start site ATG. Hypoxia upregulated CNTNAP2 by interacting with functional hypoxia response elements in CNTNAP2 promoter. Conclusion: Intermittent hypoxia enhanced sociability and working memory associated with CNTNAP2 upregulation. Our study provides novel insights into intermittent hypoxia's impact on development and the interaction between genetic and environmental risk factors in ASD pathogenesis.
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