Defining persisting brain injury after eclampsia and identifying new treatment targets to protect the maternal brain

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 available treatment but it has serious side effects, only protects from seizures in 50% of cases, and long-term neuroprotection has not been shown. Women with eclampsia run an increased risk of long-term neurological sequelae.

There is an urgent need to understand this relationship and determine pathophysiological pathways to identify how the acute injury leads to chronic sequelae and identify new targets for neuroprotective drugs.My aim is to determine recovery from the acute cerebral complications of eclampsia at six months postpartum follow-up and identify and characterize pathways that can lead to neurological injury.

I will achieve the aim by elucidating mechanisms of blood brain barrier injury, impaired cerebral blood flow autoregulation, neuroinflammation, cognitive function and sub-clinical cerebral infarcts.

I will evaluate these outcomes in women with eclampsia from my site in South Africa, as well as a rat model, and an in vitro model of preeclampsia at the University of Gothenburg, Sweden.

I will test neuroprotective treatments in rat model of preeclampsia to find new neuroprotective treatments that could improve maternal outcomes.