ArticleCNS neuroscience & therapeutics2022
Dehydroepiandrosterone alleviates hypoxia-induced learning and memory dysfunction by maintaining synaptic homeostasis.
Article in CNS neuroscience & therapeutics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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8 citing papers in PubMed, 16 citations in OpenAlex.
- Risperidone induces osteoporosis and neuropsychiatric treatment resistance via SMPD1-lysosome-mediated ferroptosis: dual rescue by active vitamin D analog ED-71.Journal of advanced research · 2026Article
- High-Altitude Hypoxia Activates JNK-p53 Signaling: Linking Hippocampal Energy Crisis to Cognitive Impairment.CNS neuroscience & therapeutics · 2026Article
- Nicotinamide Riboside Alleviates the Neurotoxic Injury of Dendritic Spine Plasticity Mediated by Hypoxic Microglial Activation.Biomolecules · 2025Article
- Androgens alleviate the depression-like phenotype in female mice by inhibiting AVPR1a in the hippocampal brain region.Molecular medicine (Cambridge, Mass.) · 2025Article
- Impact of hypoxia on the hippocampus: A review.Medicine · 2025Review
- Copper supplementation alleviates hypoxia‑induced ferroptosis and oxidative stress in neuronal cells.International journal of molecular medicine · 2024Article
- Targeting Cell Senescence and Senolytics: Novel Interventions for Age-Related Endocrine Dysfunction.Endocrine reviews · 2024Review
- Dehydroepiandrosterone alleviates hypoxia-induced learning and memory dysfunction by maintaining synaptic homeostasis.CNS neuroscience & therapeutics · 2022Article
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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
aimsHypoxia causes plenty of pathologies in the central nervous system (CNS) including impairment of cognitive and memory function. Dehydroepiandrosterone (DHEA) has been proved to have therapeutic effects on CNS injuries by maintaining the homeostasis of synapses, yet its effect on hypoxia-induced CNS damage remains unknown.
methodsIn vivo and in vitro models were established. Concentrations of glutamate and γ GABA were tested by ELISA. Levels of synapse-associated proteins were measured by western blotting. Density of dendritic protrusions of hippocampal neurons was assessed by Golgi staining. Immunofluorescence was adopted to observe the morphology of primary neurons. The novel object recognition test (NORT) and shuttle box test were used to evaluate cognition.
resultsDehydroepiandrosterone reversed abnormal elevation of glutamate levels, shortenings of neuronal processes, decreases in the density of dendritic protrusions, downregulation of synaptosome-associated protein (SNAP25), and impaired cognition caused by hypoxia. Hypoxia also resulted in notably downregulation of syntaxin 1A (Stx-1A). Overexpression of Stx-1A dramatically attenuated hypoxia-induced elevation of glutamate. Treatment with DHEA reversed the Stx-1A downregulation caused by hypoxic exposure.
conclusionDehydroepiandrosterone may exert a protective effect on hypoxia-induced memory impairment by maintaining synaptic homeostasis. These findings offer a novel understanding of the therapeutic effect of DHEA on hypoxia-induced cognitive dysfunction.
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