A5073398585- Neonatal and fetal brain pathology
- Anesthesia and Neurotoxicity Research
- Neonatal Respiratory Health Research
- Neuroinflammation and Neurodegeneration Mechanisms
- Mitochondrial Function and Pathology
- Preterm Birth and Chorioamnionitis
- Neurogenesis and neuroplasticity mechanisms
- MicroRNA in disease regulation
- Metabolism and Genetic Disorders
- Infant Development and Preterm Care
- Neuroscience of respiration and sleep
- Traumatic Brain Injury and Neurovascular Disturbances
- RNA Research and Splicing
- Diet and metabolism studies
- Phenothiazines and Benzothiazines Synthesis and Activities
- Quinazolinone synthesis and applications
- Birth, Development, and Health
- Infant Nutrition and Health
- Neuropeptides and Animal Physiology
- S100 Proteins and Annexins
- Synthesis and biological activity
- Neuroscience and Neuropharmacology Research
- Thermal Regulation in Medicine
- Nerve injury and regeneration
- Genetics and Neurodevelopmental Disorders
Université Paris Cité
2014-2024
Inserm
2014-2024
NeuroDiderot
2016-2024
Délégation Paris 7
2012-2022
Hôpital Robert-Debré
1999-2022
John Wiley & Sons (United States)
2021
Hudson Institute
2021
PremUP
2009-2019
Centre de Recherche de l'Institut de Démographie de l'Université Paris 1
2009-2019
Sorbonne Paris Cité
2011-2018
Brain-derived neurotrophic factor (BDNF) plays a prominent role in neuroprotection against perinatal brain injury. Dexmedetomidine, selective agonist of α2-adrenergic receptors, also provides glutamate-induced damage. Because adrenergic receptor agonists can modulate BDNF expression, our goal was to examine whether dexmedetomidine's neuroprotective effects are mediated by modulation mouse injury.The protective injury and dexmedetomidine alone or combination with either neutralizing antibody...
Microglia of the developing brain have unique functional properties but how their activation states are regulated is poorly understood. Inflammatory microglia in still-developing preterm-born infants associated with permanent neurological sequelae 9 million every year. Investigating regulators microglial across models neuroinflammation-mediated injury (mouse, zebrafish) and primary human mouse we found using analysis genes proteins that a reduction Wnt/β-catenin signalling necessary...
Abstract Intracerebral injection of ibotenate into mouse pups induced grey matter lesions and white cysts; co‐administration brain‐derived neurotrophic factor (BDNF) produced a dose‐dependent reduction in these lesions. In contrast, glial cell line‐derived (GDNF) had no significant effect, whereas nerve growth (NGF) or interleukin‐1β (IL‐1β) resulted exacerbation. The neuroprotective effects BDNF were abolished by anti‐BDNF antibody MEK inhibitors, ABT‐737, BH3 mimetic Bcl‐2 antagonist....
The cognitive and behavioural deficits caused by traumatic brain injury (TBI) to the immature are more severe persistent than TBI in mature brain. Understanding this developmental sensitivity is critical as children under four years of age sustain frequently any other group. Microglia (MG), resident immune cells that mediate neuroinflammation, activated following However, type temporal profile activation consequences altering it still largely unknown. In a mouse model closed head weight drop...
Perinatal brain injury is a major cause of neurodevelopmental handicaps. Multiple pathways oxidant stress, inflammation, and excitotoxicity lead to cell damage death, including caspase-dependent apoptosis. Caspase-2 (Casp2; Nedd-2, Ich-1) developmentally regulated initiator caspase, which poorly cleaves other caspases but can initiate mitochondrial outer membrane permeabilization. We have investigated if Casp2 could mediate perinatal ischemic damage.Casp2 expression in human neonatal brains...
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Brain lesions induced in newborn mice or rats by the glutamatergic agonists ibotenate (acting on NMDA and metabotropic receptors) S-bromowillardiine AMPA-kainate mimic some aspects of white matter cysts transcortical necrosis observed human perinatal brain damage associated with cerebral palsy. Exogenous endogenous cannabinoids have received increasing attention as potential neuroprotective agents a number neurodegenerative disorders adult. One recent study showed neuroprotection cannabinoid...
Brain protection of the newborn remains a challenging priority and represents totally unmet medical need. Pharmacological inhibition caspases appears as promising strategy for neuroprotection. In translational perspective, we have developed pentapeptide-based group II caspase inhibitor, TRP601/ORPHA133563, which reaches brain, inhibits activation, mitochondrial release cytochrome c, apoptosis in vivo. Single administration TRP601 protects rodent brain against excitotoxicity,...
Cerebral palsy (CP) is the most frequent neurological disorder associated with perinatal injury of developing brain. Major brain lesions CP are white matter damage (WMD) in preterm infants and cortico-subcortical term newborns. Cell therapy considered promising for repair damage. Human umbilical cord blood mononuclear cells (hUCB-MNCs) a rich source various stem that could be interest repairing Our goal was to investigate potential hUCB-MNCs prevent or an animal model excitotoxic injury. We...
Cerebral palsy (CP) is the most common motor disability in childhood, with a worldwide prevalence of 1.5-4/1,000 live births. Hypoxic-ischemic encephalopathy (HIE) contributes to burden CP, but long-term neuropathological findings this association remain limited.Thirty-four term Macaca nemestrina macaques were included study: 9 control animals delivered by cesarean section and 25 perinatal asphyxia after 15-18 min umbilical cord occlusion (UCO). UCO randomized saline (n = 11), therapeutic...
Objectives In the premature newborn, perinatal inflammation mediated by microglia contributes significantly to neurodevelopmental injuries including white matter injury (WMI). Brain alters development through neuroinflammatory processes activation of homeostatic toward a pro‐inflammatory and neurotoxic phenotype. Investigating immune regulators microglial is crucial find effective strategies prevent treat WMI. Methods Ex vivo cultures mouse model WMI induced (interleukin‐1‐beta [IL‐1β]...
Abstract Preterm infants often show pathologies of the cerebellum, which are associated with impaired motor performance, lower IQ and poor language skills at school ages. Using a mouse model inflammation‐induced encephalopathy prematurity driven by systemic administration pro‐inflammatory IL‐1β, we sought to uncover causes cerebellar damage. In this model, IL‐1β is administered between postnatal day (P) 1 5, timing equivalent last trimester for brain development in humans. Structural MRI...
Hypothermia (HT) by whole body (WBC) or selective head cooling (SHC) reduces hypoxic‐ischemic (HI) brain injury; however, whether prolonged hypothermia and/or anesthesia disrupts immature development, eg, increases apoptosis, is unknown. Anesthesia apoptosis in animals. We investigated neuroprotective and normal development. Thirty‐eight pigs <24 h old were randomized between five groups killed after 72 h: eighteen received a global insult under anesthesia, eight subsequently cooled SHC...
Apoptosis-inducing factor (AIF) deficiency compromises oxidative phosphorylation. Harlequin mice, in which AIF is downregulated, develop a severe mitochondrial complex I (CI) deficiency, suggesting that mice may represent natural model of the most common phosphorylation disorders. However, brain phenotype specifically involves cerebellum, whereas human CI deficiencies often manifest as multifocal neuropathologies. To evaluate whether this can be used to study CI-deficient disorders, whole...
Abstract Westernization of dietary habits has led to a progressive reduction in intake n‐3 polyunsaturated fatty acids (n‐3 PUFAs). Low maternal PUFAs been linked neurodevelopmental disorders, conditions which myelination processes are abnormal, leading defects brain functional connectivity. Only little is known about the role oligodendrocyte physiology and white matter development. Here, we show that lifelong PUFA deficiency disrupts oligodendrocytes maturation during postnatal period mice....
2-Alkylamino-substituted-1,4-benzoxazine derivatives, a new class of potential neuroprotective agents, were synthesized and examined for their intrinsic cytotoxicity capacity to inhibit oxidative stress-mediated neuronal degeneration in vitro. Through structure−activity relationship studies, the 3,3-diphenyl-substituted-1,4-benzoxazine derivative 3l was identified as optimal candidate, owing its potent activity, without manifestation cytotoxicity. Accordingly, proved be effective an animal...