Pierre Gressens

Dr. Pierre Gressens 
INSERM UMR 676, Université Paris-Diderot
PRES Sorbonne Paris-Cité, Hôpital Robert Debré
Assistance Publique-Hôpitaux de Paris, Paris, France. 
E-mail: p.gressens@imperial.ac.uk
E-mail: pierre.gressens@inserm.fr
Phone: +33 1 40 03 19 76 

Research Officer (DR2 Inserm) and Director, UMR 676 Inserm-Paris 7 University, Robert-Debré Hospital, Paris, France.
Professor of Perinatal Neurology, Hammersmith Hospital, ICL, London, UK.

Neurological handicap (motor or cognitive) of a perinatal origin is a serious public health problem, with increasing incidence in developed countries. This evolution notably arises from the increase in the frequency of premature newborns and in their rate of survival. This handicap is the functional consequence of perinatal brain damage, the pathophysiology of which is still poorly understood. At present, there is no known preventive treatment or cure.

Our objective is to study the pathophysiological mechanisms of brain damage in the newborn and to develop strategies for neuroprotection. These axes of research involve experimental studies in animals, and where possible, studies in humans, leading to the mutual enrichment of these two complementary approaches within a translational research framework. Evaluation of the neuroprotective effects of melatonin in the premature infant at high risk for brain damage.

Perinatal Asphyxia and Neuroinflammation in the Encephalopathy of Prematurity

Preterm birth, neonatal encephalopathy and neuroinflammation are important risk factors for the development of cerebral palsy. Inflammation is mediated by cytokines derived from immune, microglial and astrocytes cells that cause injury to neurons and oligodendrocytes. The inflammatory response affects brain development increasing the risk of neurologic diseases. One important step for improving morbidity is an increase in our knowledge to decipher the pathogenesis of injury to white matter and subplate region in the perinatal brain injury. Many factors contribute to disease progression through infectious and/or inflammatory, and hypoxic-ischemic insults. However, the mechanisms involved in the pathophysiology and severe outcome of premature babies have not been fully elucidated. Thus, the identification of biomarkers in the disease course as well as new therapeutic targets are needed in an attempt to reduce inflammatory signals and consequently the morbidity and lethality. The absence of adequate therapeutic approaches for the treatment of the encephalopathy of prematurity is due to our limited knowledge of the molecular targets that underlie the crosstalk between the neurologic and immune systems.