Tom J Phillips, Hannah Scott, David A Menassa, Ashleigh L Bignell, Aman Sood, Jude S Morton, Takami Akagi, Koki Azuma, Mark F Rogers, Catherine E Gilmore, Gareth J Inman, Simon Grant, Yealin Chung, Mais M Aljunaidy, Christy-Lynn Cooke, Bruno R Steinkraus, Andrew Pocklington, Angela Logan, Gavin P Collett, Helena Kemp, Peter A Holmans, Michael P Murphy, Tudor A Fulga, Andrew M Coney, Mitsuru Akashi, Sandra T Davidge, C Patrick Case
Some neuropsychiatric disease, including schizophrenia, may originate during prenatal development, following periods of gestational hypoxia and placental oxidative stress. Here we investigated if gestational hypoxia promotes damaging secretions from the placenta that affect fetal development and whether a mitochondria-targeted antioxidant MitoQ might prevent this. Gestational hypoxia caused low birth-weight and changes in young adult offspring brain, mimicking those in human neuropsychiatric disease. Exposure of cultured neurons to fetal plasma or to secretions from the placenta or from model trophoblast barriers that had been exposed to altered oxygenation caused similar morphological changes...
August 22, 2017: Scientific Reports