Role of microglial metabolism in perinatal neuroinflammation


Premature birth is the commonest cause of death and disability in children under the age of 5 years. In resource high settings, up to 7% of births are preterm of which 10% develop cerebral palsy, and 35% suffer neuro-behavioural deficits. Exposure to systemic inflammation is a leading cause of preterm birth and damage to the brain of preterm infants. Systemic inflammatory products signal across the endothelium and activate microglia. Microglia-driven neuroinflammation plays a key role in neurological consequences of prematurity. Understanding the molecular pathways that drive microglia into a particular activation state is essential in order to intervene in a targeted way with microglia driven neuroinflammation. We hypothesize that the metabolic paths that are active in microglia vary with the particular activation state of these cells. In addition, certain metabolic pathways may determine microglia differentiation to shape the effector function of these cells. Consequently, manipulating these pathways may constitute a novel target to combat neurological disorders with an excessive inflammatory reaction. Besides in vitro approaches, an in vivo model of brain injury of prematurity based on systemic inflammation will be used to study the importance of metabolic pathways for the activation status of microglia and the neuroinflammatory response.


Pharmacology, (epi)genetic approaches, "omics" approaches, metabolomics, extracellular vesicles isolation

Call topic


Proposed runtime

2014 - 2018

Project team

Gressens (Coordinator)
France (ANR)
Belgium (FWO)
Italy (MOH)
Sweden (SRC)