Effect of Maternal Depression on Brain-derived Neurotrophic Factor Levels in Fetal Cord Blood

Sönmez, Erdem Önder; Uğuz, Faruk; Sahingoz, Mine; Sönmez, Gülsüm; Kaya, Nazmiye; Camkurt, Mehmet Akif; Gökmen, Zeynel; Başaran, Mustafa; Gezginç, Kazım; Erdem, Sami; Dulger, Hasan Haluk; Tasyurek, Erkan

doi:10.9758/cpn.2019.17.2.308

Cited by 15 publications

(9 citation statements)

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“…A small number of studies have reported on maternal or fetal serum BDNF levels (see Supplementary Table 1 25 – 46 ). Lower maternal BDNF has been associated with postnatal depression symptoms 46 and lower cord blood BDNF associated with major depression in pregnancy 39 but other studies report no association 33 , 37 . Two studies reported a relationship between cord blood serum BDNF and maternal anxiety symptoms, again with contrasting findings 33 , 42 .…”

Section: Introductionmentioning

confidence: 97%

The placenta protects the fetal circulation from anxiety-driven elevations in maternal serum levels of brain-derived neurotrophic factor

et al. 2021

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Brain-derived neurotrophic factor (BDNF) plays crucial roles in brain function. Numerous studies report alterations in BDNF levels in human serum in various neurological conditions, including mood disorders such as depression. However, little is known about BDNF levels in the blood during pregnancy. We asked whether maternal depression and/or anxiety during pregnancy were associated with altered serum BDNF levels in mothers (n = 251) and their new-born infants (n = 212). As prenatal exposure to maternal mood disorders significantly increases the risk of neurological conditions in later life, we also examined the possibility of placental BDNF transfer by developing a new mouse model. We found no association between maternal symptoms of depression and either maternal or infant cord blood serum BDNF. However, maternal symptoms of anxiety correlated with significantly raised maternal serum BDNF exclusively in mothers of boys (r = 0.281; P = 0.005; n = 99). Serum BDNF was significantly lower in male infants than female infants but neither correlated with maternal anxiety symptoms. Consistent with this observation, we found no evidence for BDNF transfer across the placenta. We conclude that the placenta protects the developing fetus from maternal changes in serum BDNF that could otherwise have adverse consequences for fetal development.

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Section: Introductionmentioning

confidence: 97%

The placenta protects the fetal circulation from anxiety-driven elevations in maternal serum levels of brain-derived neurotrophic factor

et al. 2021

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“…However, understanding the impact of DNA methylation states of BDNF is still crucial for understanding BDNF expression modulating the underlying neurophysiology of psychiatric illnesses. Like CRH, GABA, and NR3C1, prenatal factors such as maternal depression may impact BDNF levels in the cord blood of neonates such that BDNF concentrations were significantly lower compared with healthy control subjects ( Sonmez et al, 2019 ). The actual impact of decreased BDNF in these newborns can only be unearthed by follow-up studies that track these children over their life span.…”

Section: Resultsmentioning

confidence: 99%

The Epigenetics of Anxiety Pathophysiology: A DNA Methylation and Histone Modification Focused Review

Persaud

Cates

2022

eNeuro

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Anxiety is one of the most common psychiatric disorders diagnosed in the United States today. Like all mental illnesses, anxiety pathology includes genetic, molecular, somatic, and behavioral characteristics. Specific brain regions implicated in anxiety include the prefrontal cortex, amygdala, hippocampus, and hypothalamus. Together, these regions regulate fear-related learning and memory processes, and are innervated by neuronal projections that use glutamate and GABA as neurotransmitters. Neurotrophic factors such as brain-derived neurotrophic factor (BDNF) are also implicated in anxiety. This review discusses the neuroepigenetics of the anxiety phenotype. While studying such changes is limited to postmortem brain studies or peripheral tissue acquisition in humans, the use of animals to model anxiety phenotypes has made epigenetic research possible. In this review, we summarize and discuss a plethora of DNA methylation, histone modification, and associated gene expression differences underscoring the anxiety phenotype. The findings we outline include expression changes of various DNA methyltransferases and changes in histone modifications that affect the hypothalamic pituitary adrenal axis and stress response as well as GABA, glutamate, and BDNF signaling in the PFC, amygdala, hypothalamus, and hippocampus. Furthermore, there have been studies showing that anxiety behaviors and biological scars from stress can be reversed using histone deacetylase inhibitors, and we discuss ideas for the future of treatment. In this review, we hope that by compiling much of the data pertaining to DNA methylation and histone modificationsin vivoanimal studies we are able to highlight potential avenues for future research despite existing limitations.

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“…During pregnancy, maternal exposure can alter the production and expression of neuropeptides that regulate fetal brain growth and development. [50] A clear understanding of the mechanisms responsible for the postnatal BW deficit and delayed reflex development of ADs exposed rats is still unclear. Thus, it is likely that multiple factors may be involved in these pathways, which requires further investigation.…”

Section: Discussionmentioning

confidence: 99%

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2023

AJP

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Background: Vilazodone (VLZ) and Vortioxetine (VOX) are newer antidepressants often used for treating major depressive disorder, but potential therapeutic safety for brain development in pregnant women is almost negligible due to paucity of clinical and non-clinical data. Objectives: The current work was planned to investigate possible linkages between neurodevelopmental delay and prenatal exposure to equivalent therapeutic doses of VLZ and VOX. Materials and Methods: Pregnant Wistar rats were orally gavaged with VLZ and VOX (1 mg/kg, and 2 mg/kg body weight [BW]) from gestation day 6 to 21. The dams delivered naturally and reared their litters until postnatal day 21 during which neurodevelopment reflexes were recorded. Results: Prenatally VLZ-and VOX-exposed rats showed significant (1) reduction in BW, (2) delay in forelimb grasping, (3) delay in the day of apparition of cliff avoidance, (4) delay in response in negative geotaxis only in VOX group, (5) deficit in grip strength, and (6) delayed eye opening. Conclusion: Our findings suggest that early life exposure to VLZ and VOX might be involved in the retardation and maturation of some reflexes which imply an existing association between early life VLZ and VOX exposure with an increased risk of developmental vulnerability.

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Effect of Maternal Depression on Brain-derived Neurotrophic Factor Levels in Fetal Cord Blood

Cited by 15 publications

References 38 publications

The placenta protects the fetal circulation from anxiety-driven elevations in maternal serum levels of brain-derived neurotrophic factor

The placenta protects the fetal circulation from anxiety-driven elevations in maternal serum levels of brain-derived neurotrophic factor

The Epigenetics of Anxiety Pathophysiology: A DNA Methylation and Histone Modification Focused Review

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