An animal model of chronic placental insufficiency: Relevance to neurodevelopmental disorders including schizophrenia

Rehn, Alexandra; Buuse, Maarten van den; Copolov, David L.; Briscoe, Todd; Lambert, Gavin; Rees, Sandra

doi:10.1016/j.neuroscience.2004.07.047

Cited by 82 publications

(65 citation statements)

References 64 publications

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“…The work by Rees et al (32) points to chronic intrauterine insults compromising the growth of neural processes and synapses throughout fetal brains. Animal studies of chronic placental insufficiency have shown some relevance to neurodevelopmental disorders, and the observed effects on brain development have also been shown to persist with age (e.g., with reduced striatal volumes in adolescence) (41). Hence, the etiological background for the relationship between birth weight and brain development in the normal population could likely be twofold: it may, to some extent, be based on normal variation in body and brain size, but it also may be based on variations in prenatal conditions, yielding differences in optimality of early brain development persisting through childhood and adolescence and likely, also adulthood.…”

Section: Discussionmentioning

confidence: 99%

Long-term influence of normal variation in neonatal characteristics on human brain development

Walhovd

Fjell

Brown³

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

166

163

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It is now recognized that a number of cognitive, behavioral, and mental health outcomes across the lifespan can be traced to fetal development. Although the direct mediation is unknown, the substantial variance in fetal growth, most commonly indexed by birth weight, may affect lifespan brain development. We investigated effects of normal variance in birth weight on MRI-derived measures of brain development in 628 healthy children, adolescents, and young adults in the large-scale multicenter Pediatric Imaging, Neurocognition, and Genetics study. This heterogeneous sample was recruited through geographically dispersed sites in the United States. The influence of birth weight on cortical thickness, surface area, and striatal and total brain volumes was investigated, controlling for variance in age, sex, household income, and genetic ancestry factors. Birth weight was found to exert robust positive effects on regional cortical surface area in multiple regions as well as total brain and caudate volumes. These effects were continuous across birth weight ranges and ages and were not confined to subsets of the sample. The findings show that (i) aspects of later child and adolescent brain development are influenced at birth and (ii) relatively small differences in birth weight across groups and conditions typically compared in neuropsychiatric research (e.g., Attention Deficit Hyperactivity Disorder, schizophrenia, and personality disorders) may influence group differences observed in brain parameters of interest at a later stage in life. These findings should serve to increase our attention to early influences.

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Section: Discussionmentioning

confidence: 99%

Long-term influence of normal variation in neonatal characteristics on human brain development

Walhovd

Fjell

Brown³

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

166

163

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“…Despite the increase in cell proliferation within the SVZ in severely GR foetuses, we know from our previous investigations that the volume of the neocortex is actually reduced in IUGR guinea pigs 1 week postnatally [8], with reductions in the volume of the basal ganglia and septal area at 8 weeks [34]. This suggests that neural precursor cells fail to differentiate and survive postnatally and/or that the growth of their processes is reduced.…”

Section: Discussionmentioning

confidence: 99%

Intrauterine Growth Restriction: Effects on Neural Precursor Cell Proliferation and Angiogenesis in the Foetal Subventricular Zone

et al. 2015

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Exposure to adverse prenatal factors can result in abnormal brain development, contributing to the aetiology of several neurological disorders. Intrauterine insults could occur during neurogenesis and gliogenesis, disrupting these events. Here we investigate the effects of chronic placental insufficiency (CPI) on cell proliferation and the microenvironment in the subventricular zone (SVZ). At 30 days of gestation (DG; term ∼67 DG), CPI was induced in pregnant guinea pigs via unilateral uterine artery ligation to produce growth-restricted (GR) foetuses (n = 7); controls (n = 6) were from the unoperated horn. At 60 DG, foetal brains were stained immunohistochemically to identify proliferating cells (Ki67), immature neurons (polysialylated neuronal cell adhesion molecule), astrocytes (glial fibrillary acidic protein), microglia (ionised calcium-binding adaptor molecule-1, Iba-1) and the microvasculature (von Willebrand factor) in the SVZ. There was no overall difference (p > 0.05) in the total number of Ki67-immunoreactive (IR) cells, the percentage of SVZ occupied by blood vessels or the density of Iba-1-IR microglia in control versus GR foetuses. However, regression analysis across both groups revealed that both the number of Ki67-IR cells and the percentage of SVZ occupied by blood vessels in the ventral SVZ were negatively correlated (p < 0.05) with brain weight. Furthermore, in the SVZ (dorsal and ventral) the density of blood vessels positively correlated (p < 0.05) with the number of Ki67-IR cells. Double-labelling immunofluorescence suggested that the majority of proliferating cells were likely to be neural precursor cells. Thus, we have demonstrated an association between angiogenesis and neurogenesis in the foetal neurogenic niche and have identified a window of opportunity for the administration of trophic support to enhance a neuroregenerative response.

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“…A permanent ligation of one uterine artery performed at mid-gestation in guinea pig causes alterations of the placenta, heart, aorta and kidneys in the offspring [67]. Moreover, growth-restricted fetuses and neonates are chronically hypoxic [68], hyperglycemic [69] and have an altered brain development [70]. A selective ligation of 30-50% of uteroplacental vessels late in gestation programs pronounced cardiovascular Doppler changes in fetuses, particularly in the ductus venosus, which partially reproduces the hemodynamic features of the IUGR condition in human fetuses [71].…”

Section: Proposed Mechanistic Pathways Of Iugrmentioning

confidence: 99%

Long-Term Follow-Up of Intrauterine Growth Restriction: Cardiovascular Disorders

Demicheva¹,

Crispi²

2013

Fetal Diagn Ther

101

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In the modern world, cardiovascular disorders are the leading cause of mortality in developed countries, which in most cases undergo a long subclinical phase that can last decades before the first clinical symptoms appear. Aside from the well-known risk factors related to lifestyle and genetics, there is growing evidence that in a proportion of cases, the predisposition to cardiovascular disease lies in prenatal life. Moreover, numerous historical cohort studies and animal models have shown a clear association between low birth weight and increased cardiovascular mortality in adulthood, including increased risk of hypertension, diabetes, dyslipidemia and coagulation disorders in children and adults. Besides premature birth, low birth weight in the majority of the cases is caused by intrauterine growth restriction (IUGR), which affects up to 10% of all births. Several clinical and experimental studies showed that IUGR fetuses present signs of cardiac dysfunction in utero that persist postnatally and may condition higher cardiovascular risk later in life. The present review discusses the importance of the long-term cardiovascular follow-up of the patients who suffered early or late IUGR in utero, particularly with regard to the long-term epidemiological studies in adults, prospective studies in children and the possible mechanisms that trigger IUGR and cardiovascular programming. Considering the high prevalence of IUGR and the progressing availability of intervention strategies, it is of the highest clinical relevance to detect cardiovascular risks as early as possible, to introduce timely preventive interventions and to adapt the lifestyle, in order to improve the long-term cardiovascular health outcome of IUGR cases.

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An animal model of chronic placental insufficiency: Relevance to neurodevelopmental disorders including schizophrenia

Cited by 82 publications

References 64 publications

Long-term influence of normal variation in neonatal characteristics on human brain development

Long-term influence of normal variation in neonatal characteristics on human brain development

Intrauterine Growth Restriction: Effects on Neural Precursor Cell Proliferation and Angiogenesis in the Foetal Subventricular Zone

Long-Term Follow-Up of Intrauterine Growth Restriction: Cardiovascular Disorders

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