Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2019 Oct:77:69-76.
doi: 10.1016/j.ijdevneu.2018.10.004. Epub 2018 Nov 2.

A perspective on pre-eclampsia and neurodevelopmental outcomes in the offspring: Does maternal inflammation play a role?

Affiliations
Review

A perspective on pre-eclampsia and neurodevelopmental outcomes in the offspring: Does maternal inflammation play a role?

Gillian M Maher et al. Int J Dev Neurosci. 2019 Oct.

Abstract

Pre-eclampsia is a leading cause of maternal death and maternal and perinatal morbidity. Whilst the clinical manifestations of pre-eclampsia often occur in late pregnancy, the molecular events leading into the onset of this disease are thought to originate in early pregnancy and result in insufficient placentation. Although the causative molecular basis of pre-eclampsia remains poorly understood, maternal inflammation is recognised as a core clinical feature. While the adverse effects of pre-eclampsia on maternal and fetal health in pregnancy is well-recognised, the long-term impact of pre-eclampsia exposure on the risk of autism spectrum disorder (ASD) in exposed offspring is a topic of on-going debate. In particular, a recent systematic review has reported an association between exposure to pre-eclampsia and increased risk of ASD, however the molecular basis of this association is unknown. Here we review recent evidence for; 1) maternal inflammation in pre-eclampsia; 2) epidemiological evidence for alterations in neurodevelopmental outcomes in offspring exposed to pre-eclampsia; 3) long-term changes in the brains of offspring exposed to pre-eclampsia; and 4) how maternal inflammation may lead to altered neurodevelopmental outcomes in pre-eclampsia exposed offspring. Finally, we discuss the implications of this for the development of future studies in this field.

Keywords: Autism; Behaviour; Cytokine; Inflammation; Maternal; Placenta; Pre-eclampsia.

PubMed Disclaimer

References

    1. A. Aguilar-Valles, G.N. Luheshi. Alterations in cognitive function and behavioral response to amphetamine induced by prenatal inflammation are dependent on the stage of pregnancy. Psychoneuroendocrinology. 36: 2011; 634-648
    1. B.T. Alexander, K.L. Cockrell, M.B. Massey, W.A. Bennett, J.P. Granger. Tumor necrosis factor-alpha-induced hypertension in pregnant rats results in decreased renal neuronal nitric oxide synthase expression. Am. J. Hypertens. 15: 2002; 170-175
    1. D.F. Benyo, A. Smarason, C.W. Redman, C. Sims, K.P. Conrad. Expression of inflammatory cytokines in placentas from women with preeclampsia. J. Clin. Endocrinol. Metab. 86: 2001; 2505-2512
    1. D. Bilder, J. Pinborough-Zimmerman, J. Miller, W. McMahon. Prenatal, perinatal, and neonatal factors associated with autism spectrum disorders. Pediatrics. 123: 2009; 1293-1300
    1. T.S. Bodnar, C. Raineki, W. Wertelecki, L. Yevtushok, L. Plotka, N. Zymak-Zakutnya, G. Honerkamp-Smith, A. Wells, M. Rolland, T.S. Woodward, C.D. Coles, J.A. Kable, C.D. Chambers, J. Weinberg. Altered maternal immune networks are associated with adverse child neurodevelopment: impact of alcohol consumption during pregnancy. Brain Behav. Immun. 73: 2018; 205-215