Microglia maintain structural integrity during fetal brain morphogenesis

Microglia (MG), the brain-resident macrophages, play major roles in health and disease via a diversity of cellular states. While embryonic MG display a large heterogeneity of cellular distribution and transcriptomic states, their functions remain poorly characterized. Here, we uncovered a role for MG in the maintenance of structural integrity at two fetal cortical boundaries. At these boundaries between structures that grow in distinct directions, embryonic MG accumulate, display a state resembling post-natal axon-tract-associated microglia (ATM) and prevent the progression of microcavities into large cavitary lesions, in part via a mechanism involving the ATM-factor Spp1. MG and Spp1 furthermore contribute to the rapid repair of lesions, collectively highlighting protective functions that preserve the fetal brain from physiological morphogenetic stress and injury. Our study thus highlights key major roles for embryonic MG and Spp1 in maintaining structural integrity during morphogenesis, with major implications for our understanding of MG functions and brain development.</p

Agenesis of corpus callosum: Prenatal diagnosis and prognosis

Introduction: Agenesis of corpus callosum (ACC) is commonly diagnosed prenatally. When isolated, it appears to carry a good prognosis but studies are often retrospective and follow-up short. We report a prospective study of 17 children (11 boys, 6 girls) with prenatally diagnosed isolated ACC. Methods: Neuropsychological evaluation was performed each year and results at the ages of 2, 4, and 6 years were compared. Results: Febrile seizures occurred in 3 patients. Median intellectual quotient (IQ) was within the normal range (80-109) and nonrelated to partial or complete ACC, sex, or febrile seizures. Lower median IQ was significantly related to low cultural status. With age, the number of children with IQ in the lower range (80-89) increased and slowness, attentional troubles, and instability appeared. Conclusion: This study demonstrates that if outcome of isolated ACC is favorable, a long follow-up is necessary: with age, IQ in the lower range and behavioral troubles are linked to difficulties in school.SCOPUS: ar.jinfo:eu-repo/semantics/publishe

Correction: Disruption of NEUROD2 causes a neurodevelopmental syndrome with autistic features via cell-autonomous defects in forebrain glutamatergic neurons

The article “Disruption of NEUROD2 causes a neurodevelopmental syndrome with autistic features via cell-autonomous defects in forebrain glutamatergic neurons”, written by Karen Runge, Rémi Mathieu, Stéphane Bugeon, Sahra Lafi, Corinne Beurrier, Surajit Sahu, Fabienne Schaller, Arthur Loubat, Leonard Herault, Stéphane Gaillard, Emilie Pallesi-Pocachard, Aurélie Montheil, Andreas Bosio, Jill A. Rosenfeld, Eva Hudson, Kristin Lindstrom, Saadet Mercimek- Andrews, Lauren Jeffries, Arie van Haeringen, Olivier Vanakker, Audrey Van Hecke, Dina Amrom, Sebastien Küry, Chana Ratner, Reena Jethva, Candace Gamble, Bernard Jacq, Laurent Fasano, Gabriel Santpere, Belen Lorente-Galdos, Nenad Sestan, Antoinette Gelot, Sylvie Giacuzz, Sandra Goebbels, Alfonso Represa, Carlos Cardoso, Harold Cremer & Antoine de Chevigny, was originally published electronically on the publisher’s internet portal on 29 June 2021 without open access. With the author(s)’ decision to opt for Open Choice the copyright of the article changed on 6 July 2021 to © The Author(s) 2021 and the article is forthwith distributed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0.SCOPUS: er.jinfo:eu-repo/semantics/publishe