ArticleResearch square2026
Early Peri-conceptional Alcohol Exposure before Implantation Disrupts Placental Development across Gestation.
Article in Research square, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
22 authors.
Funding
Abstract
Fetal Alcohol Spectrum Disorder, caused by prenatal alcohol exposure, remains a major public health concern, affecting up to 1 in 20 U.S. schoolchildren. As pregnancy is typically not recognized until five to six weeks of gestation, alcohol exposure often occurs unknowingly during the peri-conceptional period, a highly vulnerable developmental window of oocyte maturation, preimplantation and peri-implantaion. During this period, rapid cellular divisions precede lineage specification and organogenesis, rendering the conceptus sensitive to environmental insults such as alcohol. The placenta is increasingly recognized as an active mediator of alcohol-induced neurodevelopmental risk through the placenta-brain axis. We characterize peri-conceptional alcohol (PCA) exposure on placental development in a mouse PCA model mimicking human drinking patterns. Single-cell transcriptomic analyses on late gestation (embryonic day E17.5) placentas revealed disruption of extracellular matrix and collagen remodeling pathways within the labyrinth, processes essential for placental vascular development and mitochondrial dysfunction. Mitochondria isolated from E17.5 placentas showed compromised respiration and oxygen consumption. We assess placental vascular and hemodynamic functions with non-invasive dynamic contrast-enhanced MRI (DCE-MRI), enabling analysis across placental compartments for longitudinal evaluation of perfusion, substrate delivery, and contractile function. We demonstrate that PCA exposure arrests placental vascularization, perfusion, and morphological maturation, with PCA-exposed placentas at E17.5 resembling naïve placentas at E14.5. PCA exposure before implantation altered long-term placental programming, resulting in impaired placental perfusion and mitochondrial functions across gestation. These findings implicate placental dysfunction as a critical mechanism in Fetal Alcohol Spectrum Disorder pathogenesis and identify extracellular matrix remodeling and mitochondria as potential therapeutic targets following PCA exposure.
Indexed as
Identifiers
What OpenQuestion holds
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.