overview: The combination of antidepressant use during pregnancy and infections that cause inflammation increases the risk of neurodevelopmental disorders, including autism, in children, new research reports.
sauce: University of Virginia
Antidepressant use during pregnancy, combined with inflammation, may increase the risk of lifelong neurodevelopmental changes in the baby’s brain, such as those linked to autism, according to the University of Virginia School of Medicine. New research suggests.
A team of UVA neuroscientists have found that commonly used antidepressants known as selective serotonin reuptake inhibitors (SSRIs) can potently interact with maternal inflammation caused by infections and other causes. In laboratory mice, this interaction caused deleterious changes in the placenta and decidua (the direct link between mother and child), affecting the developing brain.
“Our findings are [SSRIs] When mixed with things like infection and inflammation, it can have detrimental consequences,” said John Lukens, Ph.D., senior research fellow at the UVA Neuroscience Division and its Brain Immunity and Glial Center (BIG) and UVA Brain. . Institute.
“Our results may help explain the rise in autism prevalence over the past two decades, as it coincides with the widespread use of SSRIs in developing countries. is.”
SSRIs during pregnancy
SSRIs are commonly used during pregnancy and are prescribed to 80% of pregnant women who need treatment for depression. Although the drug is widely considered a safe option for managing depression in pregnant women, it may increase the chance of premature birth and increase the risk of neurological and other health problems in children. There is some evidence that there is.
Lukens and his colleagues found that SSRIs interact with the mother’s immune system to trigger a strong inflammatory response at the maternal-fetal interface, the physical link between mother and offspring during pregnancy. I discovered that
The offspring of inflammation-exposed mothers later showed changes in gender-based behavior similar to those seen in people with autism, such as decreased communication and decreased interest in social interactions. Such mouse models are widely used as important autism research tools.
“We identified placental inflammatory signatures that correlated with neurological changes in adult offspring of mothers who encountered immune compromise during pregnancy,” says researcher Christine, lead author of a new scientific paper outlining the findings. Sengeller says.
“These features may help identify biomarkers and druggable targets that can help mitigate the neurodevelopmental effects of prenatal environmental stressors, such as immune responses.”
Previous research has shown that infections, autoimmune diseases, and other conditions that alter the mother’s immune status during pregnancy can affect neurodevelopment. UVA researchers believe that SSRIs can interact with and amplify that inflammation, leading to lasting brain changes.
The results make sense, the researchers say, given how SSRIs alter serotonin in the body. Serotonin is an important mood regulator, often thought of as a “feel good” chemical in the brain, but it is also an important regulator of the body’s immune response. You receive serotonin only from your mother through the placenta, so disrupting your mother’s serotonin levels can affect your baby as well.
Researchers found that inflammation alone and in combination with SSRIs reversed changes in placental serotonin levels. “We found that mothers who encountered immune disorders during pregnancy showed a completely different placental signature when using SSRIs compared to mothers who did not use SSRIs.
“This highlights the importance of considering the entire prenatal environment. Drugs designed to reduce inflammation have unintended consequences for babies when combined with other modulators such as SSRIs.” Because it is possible.”
The researchers noted that SSRIs are an important tool for managing depression and emphasized that pregnant women should not stop using SSRIs without consulting their doctor. Instead, scientists are calling for additional studies, ultimately in humans, to determine how drugs affect mothers and babies and to better understand the interactions between SSRIs and inflammation. increase.
“Untreated maternal stress, depression, and anxiety can all disrupt the neurodevelopment of offspring and adversely affect behavioral and cognitive outcomes,” the researchers wrote. It is of utmost importance to consider both the relative benefits and potential outcomes of SSRIs as a treatment option for .
The researchers published their findings in the journal Brain, Behavior, ImmunityLukens’ lab also recently discovered that it may hold the key to boosting the brain’s ability to fight Alzheimer’s disease and multiple sclerosis.
About this Pregnancy and Neurodevelopmental Research News
author: press office
sauce: University of Virginia
contact: Press Office – University of Virginia
image: image is public domain
See also
Original research: open access.
“SSRI treatment modifies the effects of maternal inflammation on intrauterine physiology and offspring neurobiologyChristine E. Zengeler and others Brain/Behavior/Immunology
overview
SSRI treatment modifies the effects of maternal inflammation on intrauterine physiology and offspring neurobiology
perturbation to intrauterine Environment can dramatically alter the neurodevelopmental trajectory of offspring. Insults commonly encountered in modern human life, such as infectious diseases, toxins, high-fat diets and prescription drugs, are increasingly associated with behavioral changes in prenatally exposed offspring.
While the potential effects of these triggers on embryonic development are being increasingly evaluated, how the critical maternal-fetal interface (MFI) responds to these various insults and how it responds. Information on how is related to altered neurodevelopment in offspring is lacking.
Here, we found that MFI responded to both inflammatory status and altered serotonergic tone in pregnant mice. Maternal immune activation (MIA) triggered an acute inflammatory response in MFI dominated by interferon signaling, compromising normal developmental-related transcriptional programs.
The major MFI compartments, the decidua and placenta, each responded differently to MIA. We also found that MFI exposed to MIA disrupted sex-specific gene expression and increased serotonin levels. I have found that I am not affected.
Moreover, combined maternal inflammation in the presence of pharmacological inhibition of serotonin reuptake further altered MFI physiology and offspring neurobiology, affecting immune and serotonin signaling pathways as well. rice field.
Altogether, these findings highlight the complexity of assessing diverse environmental influences on placental physiology and neurodevelopment.
