Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Neuronal miR-17-5p contributes to interhemispheric cortical connectivity defects induced by prenatal alcohol exposure

22 Aug 2023

Abstract excerpt

Structural and functional deficits in brain connectivity are reported in patients with fetal alcohol spectrum disorders (FASDs), but whether and how prenatal alcohol exposure (PAE) affects axonal development of neurons and disrupts wiring between brain regions is unknown. Here, we develop a mouse model of moderate alcohol exposure during prenatal brain wiring to study the effects of PAE on corpus callosum (CC)...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Birth, Development, and Health
Share to Neonatal and fetal brain pathology
Share to Prenatal Substance Exposure Effects

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 37610874
DOI: 10.1016/j.celrep.2023.113020

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Neuronal miR-17-5p contributes to interhemispheric cortical connectivity defects induced by prenatal alcohol exposurePMID 37610874Read ↗

Neuronal miR-17-5p contributes to interhemispheric cortical connectivity defects induced by prenatal alcohol exposureSemantic proximity Read ↗

Transcriptomic changes due to early, chronic intermittent alcohol exposure during forebrain development implicate WNT signaling, cell‐type specification, and cortical regionalization as primary determinants of fetal alcohol syndromeSemantic proximity Read ↗

Transcriptomic changes due to early, chronic alcohol exposure during cortical development implicate regionalization, cell-type specification, synaptogenesis and WNT signaling as primary determinants of fetal alcohol Spectrum DisordersSemantic proximity Read ↗

Prenatal Ethanol Exposure and Neocortical Development: A Transgenerational Model of FASDSemantic proximity Read ↗

Prenatal Ethanol Exposure Disrupts Intraneocortical Circuitry, Cortical Gene Expression, and Behavior in a Mouse Model of FASDSemantic proximity Read ↗

Acute oligodendrocyte loss with persistent white matter injury in a third trimester equivalent mouse model of fetal alcohol spectrum disorderSemantic proximity Read ↗

Neurodevelopmental alcohol exposure elicits long-term changes to gene expression that alter distinct molecular pathways dependent on timing of exposureSemantic proximity Read ↗

Fetal Alcohol Spectrum Disorder: Potential Role of Endocannabinoids SignalingSemantic proximity Read ↗

Neurodevelopmental Trajectories Following Prenatal Alcohol ExposureSemantic proximity Read ↗

Fetal Alcohol Spectrum Disorders: An Overview from the Glia PerspectiveSemantic proximity Read ↗

Combined transcriptome analysis of fetal human and mouse cerebral cortex exposed to alcoholSemantic proximity Read ↗

An overview of current advances in perinatal alcohol exposure and pathogenesis of fetal alcohol spectrum disordersSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.