ArticleAlcohol (Fayetteville, N.Y.)2009
Ethanol inhibition of aspartyl-asparaginyl-beta-hydroxylase in fetal alcohol spectrum disorder: potential link to the impairments in central nervous system neuronal migration.
Article in Alcohol (Fayetteville, N.Y.), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 58 citations in OpenAlex.
- Article
- Article
- Impact of Prenatal Dietary Soy on Cerebellar Neurodevelopment and Function in Experimental Fetal Alcohol Spectrum Disorder.Nutrients · 2025Article
- Dietary Soy Preserves Cognitive Function in Experimental Fetal Alcohol Spectrum Disorder: Role of Increased Signaling through Notch and Gonadotropin Releasing Hormone Networks.Journal of behavioral and brain science · 2025Article
- Chondrosarcoma: Adjuvant Therapeutic Effects of the ASPH Small Molecule Inhibitor, SMI-1182, With Doxorubicin.Japanese journal of cancer and oncology research · 2025Article
- Brain and Serum Membrane Vesicle (Exosome) Profiles in Experimental Alcohol-Related Brain Degeneration: Forging the Path to Non-Invasive Liquid Biopsy Diagnostics.Journal of molecular pathology · 2024Article
- The Impact of Prenatal Alcohol Exposure on Longitudinal Growth, Nutritional Status, and Insulin-Like Growth Factor 1 in Early Childhood in Leyte, the Philippines.The Journal of pediatrics · 2024Article
- An overview of current advances in perinatal alcohol exposure and pathogenesis of fetal alcohol spectrum disorders.Journal of neurodevelopmental disorders · 2024Review
- Agent Orange Herbicidal Toxin-Initiation of Alzheimer-Type Neurodegeneration.Journal of Alzheimer's disease : JAD · 2024Article
- Association between dietary soy prevention of fetal alcohol spectrum disorder and normalization of placental insulin and insulin-like growth factor signaling networks and downstream effector molecule expression.Gene & protein in disease · 2024Article
- Early-Stage Moderate Alcohol Feeding Dysregulates Insulin-Related Metabolic Hormone Expression in the Brain: Potential Links to Neurodegeneration Including Alzheimer's Disease.Journal of Alzheimer's disease reports · 2024Article
- Differential Early Mechanistic Frontal Lobe Responses to Choline Chloride and Soy Isoflavones in an Experimental Model of Fetal Alcohol Spectrum Disorder.International journal of molecular sciences · 2023Article
- Agent Orange Causes Metabolic Dysfunction and Molecular Pathology Reminiscent of Alzheimer's Disease.Journal of Alzheimer's disease reports · 2023Article
- Differential rescue effects of choline chloride and soy isolate on metabolic dysfunction in immature central nervous system neurons: Relevance to fetal alcohol spectrum disorder.Diabetes management (London, England) · 2023Article
- Dietary Soy Prevents Alcohol-Mediated Neurocognitive Dysfunction and Associated Impairments in Brain Insulin Pathway Signaling in an Adolescent Rat Model.Biomolecules · 2022Article
- Article
- Ethanol-Induced White Matter Atrophy Is Associated with Impaired Expression of Aspartyl-Asparaginyl-Journal of drug and alcohol research · 2017Article
- Aspartate-β-hydroxylase (ASPH): A potential therapeutic target in human malignant gliomas.Heliyon · 2016Article
- Tobacco Nitrosamine Exposures Contribute to Fetal Alcohol Spectrum Disorder Associated Cerebellar Dysgenesis.International journal of biology · 2016Article
- Potential Co-Factor Role of Tobacco Specific Nitrosamine Exposures in the Pathogenesis of Fetal Alcohol Spectrum Disorder.Gynecology and obstetrics research : open journal · 2016Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Fetal alcohol spectrum disorder (FASD) is caused by prenatal exposure to alcohol and associated with hypoplasia and impaired neuronal migration in the cerebellum. Neuronal survival and motility are stimulated by insulin and insulin-like growth factor (IGF), whose signaling pathways are major targets of ethanol neurotoxicity. To better understand the mechanisms of ethanol-impaired neuronal migration during development, we examined the effects of chronic gestational exposure to ethanol on aspartyl (asparaginyl)-beta-hydroxylase (AAH) expression, because AAH is regulated by insulin/IGF and mediates neuronal motility. Pregnant Long-Evans rats were pair-fed isocaloric liquid diets containing 0, 8, 18, 26, or 37% ethanol by caloric content from gestation day 6 through delivery. Cerebella harvested from postnatal day 1 pups were used to examine AAH expression in tissue, and neuronal motility in Boyden chamber assays. We also used cerebellar neuron cultures to examine the effects of ethanol on insulin/IGF-stimulated AAH expression, and assess the role of GSK-3beta-mediated phosphorylation on AAH protein levels. Chronic gestational exposure to ethanol caused dose-dependent impairments in neuronal migration and corresponding reductions in AAH protein expression in developing cerebella. In addition, prenatal ethanol exposure inhibited insulin and IGF-I-stimulated directional motility in isolated cerebellar granule neurons. Ethanol-treated neuronal cultures (50mMx96h) also had reduced levels of AAH protein. Mechanistically, we showed that AAH protein could be phosphorylated on Ser residues by GSK-3beta, and that chemical inhibition of GSK-3beta and/or global Caspases increases AAH protein in both control- and ethanol-exposed cells. Ethanol-impaired neuronal migration in FASD is associated with reduced AAH expression. Because ethanol increases the activities of both GSK-3beta and Caspases, the inhibitory effect of ethanol on neuronal migration could be mediated by increased GSK-3beta phosphorylation and Caspase degradation of AAH protein.
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Registered trials
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