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Early and late effects of perinatal exposure to Bisphenol A on hippocampal development

Widely used in consumer goods, Bisphenol A (BPA) has raised widespread safety concerns, especially for fetuses and infants. By using sensitive cellular indicators to examine the effects of BPA on the development of the mouse hippocampus, Dr. Christina Chatzi’s innovative approach aims to uncover endocrine disruption or neurotoxicity affecting life-long learning and memory. In addition to advancing understanding of the effects of BPA, the approach should apply to other environmental risks to brain development.

The risks of Bisphenol A on brain development

In her own words...

I’m Dr Chatzi and I work at the Université de Liège on the impact of Bisphenol A (BPA) on the development of the brain of new-born.
My research has been supported by the AXA Research Fund since 2012.
Biology and Chemistry were my favorite subjects throughout school. But I specifically remember being blown away at 14 years old after reading a small book on HIV and retrovirus replication cycle I found on my older sister’s desk (a medical student then). The idea of looking at biology from the bottom up and asking how things work at a molecular and cellular level fascinated me. Later on, at the end of my Master of Science degree, I became really interested in developmental biology and decided that I would like to study how environmental and genetic cues may determine cell growth, differentiation and morphogenesis.

What is Bisphenol A and how are we exposed?
Bisphenol A (BPA) has been identified as an Endocrine Disrupting Chemical that is potentially harmful for neurological development. This ubiquitous industrial chemical, used in the manufacture of plastics and epoxy resins, can be found in plastic bottles, baby bottles, and food cans, and is detected in the urine of greater than 90% of Americans and Europeans including pregnant women.
Fetuses and newborns seem to be particularly vulnerable because BPA crosses the placenta. Several studies have reported impaired cognitive performances in rodents perinatally exposed to BPA at low doses, and human studies suggest that exposure to BPA could alter cognition and behavior.

Why do you study its effect on new-born?

Given the crucial role of sex steroids and thyroid hormones in the development of neurons, we hypothesize that alterations of hormonal functions by endocrine disrupters early in life could have life-long consequences on brain function.
We examine the effect of BPA on the development of synapses and circuits in the mouse hippocampus, a brain structure vital to learning and memory. The formation of new neurons in the hippocampus is most intense during the first postnatal week, but continues throughout life and is influenced by estradiol and thyroid hormones. We hypothesize that perinatal BPA-mediated disruption of sex steroid or thyroid hormones affects the formation of new neurons in the hippocampus.
One of our main aims is to determine whether perinatal exposure to BPA affects the birth of new neurons and the formation of functional circuits in the hippocampus of infant mice.
Additionally, we examine whether perinatal exposure to BPA causes persistent effects on new neurons born later during adult life.

Bisphenol A has already been banned by some governments. What will your research bring to the public debate on risks related to Bisphenol A?

Many environmental agencies have underlined the necessity to determine whether early exposure to BPA alters brain development. Sex steroids and thyroid hormones play a major role in brain development thus alteration of hormonal functions by BPA could lead to deficiencies in learning and memory. This is a major question for Society.
We will study the effects of exposure to BPA during pregnancy and early postnatal life. Furthermore, we will try to see whether early exposure to BPA could lead to deleterious effects later in adult life. For this, we will use doses of BPA that are environmentally relevant. This should bring more information on the risks of BPA. The models we will develop could also be extended to other endocrine disrupters for which there is no regulation yet.

To add or modify information on this page, please contact us at the following address: community.research@axa.com

Christina
CHATZI

Institution

Université de Liège

Country

Belgium

Nationality

Belgian

ORCID Open Researcher and Contributor ID, a unique and persistent identifier to researchers