2 research outputs found
Erratum to âN-3 PUFA deficiency disrupts oligodendrocyte maturation and myelin integrity during brain developmentâ
This article corrects the following:N-3 PUFA deficiency disrupts oligodendrocyte maturation and myelin integrity during brain developmentQuentin Leyrolle, Fanny Decoeur, Cyril Dejean, Galadriel BriÚre, Stephane Leon, Ioannis Bakoyiannis, Emilie Baroux, Tony-Lee Sterley, Clémentine Bosch-Bouju, Lydie Morel, Camille Amadieu, Cynthia Lecours, Marie-Kim St-Pierre, Maude Bordeleau, Helene Roumes, Véronique De Smedt-Peyrusse, Alexandran Séré, Leslie Schwendimann, Stephane Grégoire, Lionel Bretillon, Niyazi Acar, Corinne Joffre, Guillaume Ferreira, Raluca Uricaru, Patricia Thebault, Pierre Gressens, Marie-Eve Tremblay, Sophie Layé, Agnes Nadjar Volume 70Issue 1Glia pages: 50-70 First Published online: September 14, 2021International audienc
Nâ3 PUFA deficiency disrupts oligodendrocyte maturation and myelin integrity during brain development
International audienceWesternization of dietary habits has led to a progressive reduction in dietary intake of n-3 polyunsaturated fatty acids (n-3 PUFAs). Low maternal intake of n-3 PUFAs has been linked to neurodevelopmental disorders, conditions in which myelination processes are abnormal, leading to defects in brain functional connectivity. Only little is known about the role of n-3 PUFAs in oligodendrocyte physiology and white matter development. Here, we show that lifelong n-3 PUFA deficiency disrupts oligodendrocytes maturation and myelination processes during the postnatal period in mice. This has long-term deleterious consequences on white matter organization and hippocampus-prefrontal functional connectivity in adults, associated with cognitive and emotional disorders. Promoting developmental myelination with clemastine, a first-generation histamine antagonist and enhancer of oligodendrocyte precursor cell differentiation, rescues memory deficits in n-3 PUFA deficient animals. Our findings identify a novel mechanism through which n-3 PUFA deficiency alters brain functions by disrupting oligodendrocyte maturation and brain myelination during the neurodevelopmental period