Project description
Defining neurological outcomes after eclampsia to inform new treatments
Preeclampsia and eclampsia are important causes of maternal mortality. Magnesium sulfate is only used in the acute setting and is effective in 50 % of cases with significant side effects. Women who experience eclampsia are at higher risk of later neurological disorders. Understanding the connection between acute and long-term complications is critical for developing new neuroprotective treatments. The ERC-funded INCENTIVE project aims to define neurological outcomes after eclampsia and identify the pathophysiological pathways. The project’s goal is to develop new neuroprotective drugs for the maternal brain. It will evaluate recovery from acute cerebral complications of eclampsia, with assessments at 6 to 12 months postpartum. Areas of investigation will include blood-brain barrier injury, cerebral blood flow autoregulation, neuroinflammation, cognitive deficits, and white matter scarring.
Objective
The goal of this project is to define neurological outcomes after eclampsia and to determine underlying pathophysiological pathways to eclampsia which will lead to new drugs for neuroprotection of the maternal brain.
Preeclampsia and eclampsia are the most common causes of direct maternal death globally. Magnesium sulphate is the only treatment in use but it has serious side effects, only protects from seizures in 50% of cases and neuroprotection on longterm is not established. Women with eclampsia run an increased risk of longterm neurological sequelae but causality with the acute insult is not proven. There is an urgent need to understand this relationship and underlying pathophysiological pathways to identify how the acute injury affects the chronic sequelae and identify new targets for neuroprotective drugs.
I want to respond to this need by determining recovery from the acute cerebral complications of eclampsia to follow up 6 months postpartum and characterize and identify pathways for neurological injury secondary to eclampsia. This will be achieved by investigating mechanisms of blood brain barrier injury, cerebral blood flow autoregulation, neuroinflammation, cognitive function deficits and white matter scarring in the brain. I will make use of a cohort of women with eclampsia from my site at Stellenbosch University, South Africa, as well as a rat model of preeclampsia and an in vitro model of preeclampsia in my lab at the University of Gothenburg, Sweden, to evaluate these outcomes. I will use anti-diabetic and anti-epileptic drugs commonly used in pregnancy and test these in rat model of preeclampsia to find new neuroprotective treatments that improve maternal outcomes. This could enable us to protect the maternal brain, save lives and reduce morbidity globally.
My position as a fully trained obstetrician conducting translational research, focusing on cerebral complications makes me unique in the field and very well fitted to conduct this research project
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Programme(s)
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HORIZON.1.1 - European Research Council (ERC)
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(opens in new window) ERC-2024-STG
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405 30 Goeteborg
Sweden
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