Glial homeostasis, neuroinflammation and neuroprotection
Pre-, peri- or post-natal cerebral lesions, caused by intrinsic (cerebrovascular accidents, tumors, etc.) or extrinsic factors (fetal or maternal infections and immune activation, head trauma, etc.) lead to severe neurological deficits such as motor, sensory or cognitive defects at the origin of communication and behavior disorders. The NeuroKines team seeks to better understand the cellular mechanisms and the role of immunity and metabolism involved in the genesis of neurological lesions during brain development in order to identify new predictive diagnostic biomarkers and therapeutic targets. The candidate molecules are tested on various in vitro, in vivo models and pediatrics cohorts, reproducing pediatric neuropathological processes, with the aim of transferring the most promising neuroprotection strategies towards clinical trials.
The NeuroKines team is made up of 6 independent groups with complementary themes and led by Pierre Gressens and Juliette Van Steenwinckel (G1), Olivier Baud (G2), Stéphane Auvin and Pascal Dournaud (G3), Nadia Soussi-Yanicostas (G4), Malgorzata Rak (G5) and Mireille Laforge (G6).
KEY WORDS: Prematurity, Epilepsy, Autism, Cognitive deficits, Neuroinflammation, Infections, Immune activation, Immune response, Immunometabolism, Energy metabolism
Roles of microglia and strategies of neuroprotection
Microglia and epilepsy in the zebrafish
Prevention of perinatal neuroinflammation
Physiopathology and therapy of mitochondrial diseases
Neuroinflammation and neurotransmission
Immunometabolism and inflammation
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