Early life stressful experiences and neuropsychiatric vulnerability: evidences from human and animal models
Med Sci (Paris). 2016-01-01; 32(1): 93-99
DOI: 10.1051/medsci/20163201015
Lire sur PubMed
Rincel M(1), Lépinay A(1), Gabory A(2), Théodorou V(3), Koehl M(4), Daugé V(5), Maccari S(6), Darnaudéry M(1).
Author information:
(1)Université de Bordeaux, Nutrition et neurobiologie intégrée (NUTRINEURO), UMR 1286, 146, rue Léo Saignat, 33076 Bordeaux Cedex, France – Inra, Nutrition et neurobiologie intégrée (NUTRINEURO), UMR 1286, F-33076 Bordeaux, France.
(2)UMR 1198, biologie du développement et reproduction, Inra – Centre de recherche de Jouy en Josas, F-78352 Jouy-en-Josas, France.
(3)Inra, UMR 1331- Toxicologie alimentaire (TOXALIM), F-31027 Toulouse, France.
(4)Neurocentre Magendie, université Bordeaux, F- 33077 Bordeaux, France.
(5)Inra, Microbiologie de l’alimentation au service de la Santé (MICALIS), UMR 1319, équipe Alimentation, microbiote intestinal, pathologies encéphaliques et métabolique (AMIPEM) F-78352, Jouy-en-Josas, France.
(6)Sapienza university of Rome/ Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS), Istituto Neurologico Merditerraneo (NEUROMED), Italie – UMR 8576 CNRS, université de Lille, France.
The human newborn is highly dependent on parental care for its survival but also for the healthy development of its brain. A large body of literature demonstrates the impact of early life adversity, even during the prenatal period, on the adult’s health. The susceptibility to neuropsychiatric diseases is often potentiated by early stress. If there is an agreement that a critical developmental period exists, the mechanisms underlying the long term effects of early life adversity are still poorly understood. Recent studies in animals highlight the involvement of epigenetic processes in the transmission of such vulnerabilities, notably via modifications in germ cells, which can be transmitted in the next generations.
© 2016 médecine/sciences – Inserm.