M. Lévy

ORCID: 0000-0003-1065-8511
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About
Contact & Profiles
Research Areas
  • Pulmonary Hypertension Research and Treatments
  • Congenital Heart Disease Studies
  • Neurogenesis and neuroplasticity mechanisms
  • Cardiovascular Issues in Pregnancy
  • Systemic Lupus Erythematosus Research
  • Neonatal Respiratory Health Research
  • Tumors and Oncological Cases
  • Cardiac Valve Diseases and Treatments
  • Liver Diseases and Immunity
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Cardiovascular Syncope and Autonomic Disorders
  • Diabetes and associated disorders
  • Respiratory Support and Mechanisms
  • Muscle Physiology and Disorders
  • Abdominal Surgery and Complications
  • Inhalation and Respiratory Drug Delivery
  • Organ and Tissue Transplantation Research
  • Quinazolinone synthesis and applications
  • Pain Management and Treatment
  • Biotin and Related Studies
  • Tryptophan and brain disorders
  • Congenital heart defects research
  • Immune cells in cancer
  • Cardiac Arrhythmias and Treatments
  • Tracheal and airway disorders

Hôpital Necker-Enfants Malades
1993-2023

Inserm
1990-2022

Université Paris Cité
2005-2022

Sorbonne Université
2020-2022

Centre National de la Recherche Scientifique
2020-2022

Institut du Cerveau
2022

Hôpital Robert-Debré
2021

Centre Hospitalier Universitaire de Bordeaux
2019

Institut de Psychiatrie et Neurosciences de Paris
2018-2019

Délégation Paris 5
2008-2019

Selective serotonin reuptake inhibitors are among the most prescribed antidepressants. Fluoxetine is lead molecule which exerts its therapeutic effects, at least in part, by promoting neuroplasticity through increased brain-derived neurotrophic factor (BDNF)/tropomyosin-related receptor kinase B (TrkB) signalling. It unclear however, to extent neuroplastic effects of fluoxetine solely mediated inhibition transporter (5-HTT). To answer this question, on were analysed both wild type (WT) and...

10.1038/s41598-019-42775-w article EN cc-by Scientific Reports 2019-04-19

10.1152/ajplegacy.1974.227.5.1084 article EN American Journal of Physiology-Legacy Content 1974-11-01

Accumulating evidences suggest a strong correlation between metabolic changes and neurodegeneration in CNS demyelinating diseases such as multiple sclerosis (MS). Biotin, an essential cofactor for five carboxylases, is expressed by oligodendrocytes involved fatty acid synthesis energy production. The effect of biotin or high-dose-biotin (MD1003) has been reported on rodent vitro, neurodegenerative animal models. However, clinical studies, showed mild no beneficial MD1003 amyotrophic lateral...

10.3390/ijms232415733 article EN International Journal of Molecular Sciences 2022-12-12

Abstract The remyelination failure in multiple sclerosis (MS) is associated with a migration/differentiation block of oligodendroglia. reason for this highly debated. It could result from disease-related extrinsic regulators the oligodendroglial biology or reflect MS oligodendrocyte intrinsic properties. To avoid confounding immune-mediated effect, we used an immune-deficient, dysmyelinating mouse model, to compare side-by-side induced pluripotent stem-cell-derived O4+ oligodendroglia and...

10.1101/2020.05.05.078642 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2020-05-06
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