ArticleJournal of molecular neuroscience : MN2004
A neuroprotective peptide antagonizes fetal alcohol exposure-compromised brain growth.
Article in Journal of molecular neuroscience : MN, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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Who cites it
19 citing papers in PubMed, 35 citations in OpenAlex.
- Article
- Neuroprotective Peptide NAPVSIPQ Antagonizes Ethanol Inhibition of L1 Adhesion by Promoting the Dissociation of L1 and Ankyrin-G.Biological psychiatry · 2020Article
- DNA Methylation program in normal and alcohol-induced thinning cortex.Alcohol (Fayetteville, N.Y.) · 2017Article
- Article
- Rehabilitation training using complex motor learning rescues deficits in eyeblink classical conditioning in female rats induced by binge-like neonatal alcohol exposure.Alcoholism, clinical and experimental research · 2013Article
- Mitogen-activated protein kinase modulates ethanol inhibition of cell adhesion mediated by the L1 neural cell adhesion molecule.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Article
- From research to practice: an integrative framework for the development of interventions for children with fetal alcohol spectrum disorders.Neuropsychology review · 2011Review
- Two alcohol binding residues interact across a domain interface of the L1 neural cell adhesion molecule and regulate cell adhesion.The Journal of biological chemistry · 2011Article
- Effects of ethanol and NAP on cerebellar expression of the neural cell adhesion molecule L1.PloS one · 2011Article
- Prenatal choline supplementation mitigates behavioral alterations associated with prenatal alcohol exposure in rats.Birth defects research. Part A, Clinical and molecular teratology · 2010Article
- Alteration of selective neurotransmitters in fetal brains of prenatally alcohol-treated C57BL/6 mice: quantitative analysis using liquid chromatography/tandem mass spectrometry.International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience · 2010Article
- A novel peptide, colivelin, prevents alcohol-induced apoptosis in fetal brain of C57BL/6 mice: signaling pathway investigations.Neuroscience · 2009Article
- Activity-dependent neuroprotective protein-derived peptide, NAP, preventing alcohol-induced apoptosis in fetal brain of C57BL/6 mouse.Neuroscience · 2009Article
- Peptidergic agonists of activity-dependent neurotrophic factor protect against prenatal alcohol-induced neural tube defects and serotonin neuron loss.Alcoholism, clinical and experimental research · 2008Article
- An alcohol binding site on the neural cell adhesion molecule L1.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
- Understanding the mechanism of learning enhancement: NMDA and GABA receptor expression.American journal of obstetrics and gynecology · 2007Article
- Protection against prenatal alcohol-induced damage.PLoS medicine · 2006Article
- Prenatal choline supplementation mitigates the adverse effects of prenatal alcohol exposure on development in rats.Neurotoxicology and teratologyArticle
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
We evaluated a 9-amino-acid peptide, SALLRSIPA (SAL), an agonist of activity-dependent neurotrophic factor (ADNF), for its protective properties against fetal alcohol-related brain growth retardation, using an established liquid diet model of alcohol-related neurodevelopmental disorder (ARND) in C57BL/6 mice. Alcohol exposure during neurulation reduced body weight, head size, and specifically brain weight and volume. Major gross brain deficits include underdevelopment of brain areas, cortical thinning, ventricle enlargement, and restricted midline neural tissue growth leading to openings at the roof/floor plate. SALLRSIPA (SAL) treatment increased fetal body weight and restored brain weight, brain volume, and regional brain size. Furthermore, SAL restored cortical thickness, reduced the size and frequency of neural tube openings, and attenuated ventricular enlargement. The ability of SAL to antagonize alcohol-retarded brain growth and development of forebrain and midline neural tube at midgestation suggests its potential use as an antagonist against fetal alcohol- rendered microencephaly early in development.
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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.