Although alcohol consumption during pregnancy is a major cause of behavioral and learning disabilities, most FASD infants remain late- or even misdiagnosed. Neuroplacentology has emerged as a new field of research focusing on the role of the placenta in fetal brain development. Several studies focusing on the pro-angiogenic factor PlGF have reported that prenatal alcohol exposure (PAE) dysregulates a functional placenta–cortex axis, leading to neurovascular-related defects. Here, we provide the first transcriptomic “placenta–cortex” signature of the effects of PAE on fetal angiogenesis. Whole mouse genome microarrays of paired placentas and cortices were performed to establish the transcriptomic inter-organ “placenta–cortex” signature in control and PAE groups at gestational day 20. A Venn analysis followed by a gene ontology analysis revealed 107 genes differentially expressed between both signatures and associated with vascular development. String protein–protein interaction analysis showed that they were associated with three functional clusters. PANTHER functional classification analysis indicated that “intercellular communication” was a significantly enriched biological process, and 27 genes were encoding neuroactive ligand/receptors interactors. Validation experiments involving Western blot in mice and immunolabeling in fetal human samples confirmed the transcriptomic data for one ligand–receptor couple (Agt/AGTR1/2). In conclusion, this study establishes the first transcriptomic placenta–cortex signature of a developing mouse and shows that PAE markedly unbalances this inter-organ signature; in particular, several ligands and/or receptors involved in the inter-organ communication and the control of angiogenesis. Such a signature would present a clinical value for early diagnosis of brain defects in FASD.