Project R-4307


Embryonic microglia as the 'missing link' in the development of neuropsychiatric disorders. (Research)


It is known that maternal infections increase the risk on autism and schizophrenia in the offspring, suggesting that prenatal immune activation could be harmful to brain development and thus be involved in the etiology of the disorders. Microglia are the resident immune cells of the central nervous system (CNS) and their activation during prenatal development possibly results in the defective establishment of neuronal circuits. The answer to this question will have an impact on the treatment of pregnant women with an infection and will be the central aim of our work. We will study the role of microglia in the development of the embryonic CNS under three conditions: normal development (healthy non-infected mothers), under conditions of maternal inflammation (prenatal activation of microglia, like a gain of function model), and in a mouse model in which all microglia are ablated (loss of function). We want to study the molecules involved in the colonization of the embryonic CNS by microglia and in the pattern of microglial migration in the cortex. We will investigate when and where during development microglia interact with neuronal precursors, neurons and blood vessels in the embryonic cortex. Our final goal is to understand the role of microglia in the development of radially migrating excitatory neurons, tangentially migrating interneurons and in the establishment of well balanced inhibitory-excitatory neuronal circuits in health and disease.

Period of project

01 January 2013 - 31 December 2016