A5066909582- Genomics and Rare Diseases
- Proteoglycans and glycosaminoglycans research
- Muscle metabolism and nutrition
- Connective tissue disorders research
- Muscle Physiology and Disorders
- Genetics and Neurodevelopmental Disorders
- Glycosylation and Glycoproteins Research
- Radiopharmaceutical Chemistry and Applications
- Anesthesia and Neurotoxicity Research
- Neonatal Respiratory Health Research
- Neonatal and fetal brain pathology
- Alzheimer's disease research and treatments
- Glaucoma and retinal disorders
- 14-3-3 protein interactions
- Cell Adhesion Molecules Research
- Cancer Immunotherapy and Biomarkers
- Protein Kinase Regulation and GTPase Signaling
- CRISPR and Genetic Engineering
- Neurological Disorders and Treatments
- Pluripotent Stem Cells Research
- Metabolism and Genetic Disorders
- Brain Metastases and Treatment
- Chemical Reactions and Isotopes
- Carbohydrate Chemistry and Synthesis
- Fibroblast Growth Factor Research
Université Paris-Saclay
2023-2024
CEA Paris-Saclay
2023-2024
Commissariat à l'Énergie Atomique et aux Énergies Alternatives
2015-2024
Laboratoire de Recherche sur la Croissance Cellulaire, la Réparation et la Régénération Tissulaires
2017-2024
Université Paris-Est Créteil
2017-2024
Technologies pour la Santé
2023
Institut National de Recherche pour l'Agriculture, l'Alimentation et l'Environnement
2023
Centre National de la Recherche Scientifique
2017-2018
Cyceron
2015
Glycosaminoglycans (GAGs), including heparan sulfates and chondroitin sulfates, are major components of the extracellular matrix. Upon interacting with heparin binding growth factors (HBGF), GAGs participate to maintaintenance tissue homeostasis contribute self-healing. Although several processes regulated by HBGF altered in Alzheimer’s disease, it is unknown whether brain GAG capacities bind regulate function or other proteins, as tau, modified this disease. Here, we show that total...
Human brain organoids (mini-brains) consist of self-organized three-dimensional (3D) neural tissue which can be derived from reprogrammed adult cells and maintained for months in culture. These 3D structures manifest substantial potential the modeling neurodegenerative diseases pave way personalized medicine. However, as these models express whole human genetic complexity, it is critical to have access isogenic mini-brains that only differ specific controlled variables. Genetic engineering...
Hypoxic-ischemic encephalopathy (HIE) is a major cause of newborn brain damage stemming from lack oxygenated blood flow in the neonatal period. Twenty-five to fifty percent asphyxiated infants who develop HIE die period, and about sixty survivors long-term neurological disabilities. From first minutes months after injury, cascade events occurs, leading blood-brain barrier (BBB) opening, neuronal death inflammation. To date, only approach proposed some cases therapeutic hypothermia (TH)....
Engrailed 1 (En1) and 2 (En2) code for closely related homeoproteins acting as transcription factors signaling molecules that contribute to midbrain hindbrain patterning, development maintenance of monoaminergic pathways, retinotectal wiring. En2 has been suggested be an autism susceptibility gene individuals with display overexpression this homeogene but the mechanisms remain unclear. We addressed in present study effect exogenously added on morphology hippocampal cells normally express...
Abstract Heparan sulfate (HS) chains, covalently linked to heparan proteoglycans (HSPG), promote synaptic development and functions by connecting various adhesion proteins (AP). HS binding AP could vary according modifications of chains different sulfotransferases. 3- O -sulfotransferases (Hs3sts) produce rare -sulfated HSs (3S-HSs), poorly known in the nervous system. Here, we showed that a peptide block herpes simplex virus interfering with 3S-HSs vitro vivo (i.e. G2 peptide), specifically...
Creatine transporter deficiency (CTD) is an X-linked disease caused by mutations in the SLC6A8 gene. The impaired creatine uptake brain results intellectual disability, behavioral disorders, language delay, and seizures. In this work, we generated human organoids from induced pluripotent stem cells of healthy subjects CTD patients. Brain donors had reduced compared with those donors. expression neural progenitor cell markers SOX2 PAX6 was CTD-derived organoids, while GSK3β, a key regulator...
Creatine transporter deficiency (CTD) is an X-linked disease caused by mutations in the SLC6A8 gene. The impaired creatine uptake brain results intellectual disability, behavioral disorders, language delay, and seizures. In this work, we generated human organoids from induced pluripotent stem cells of healthy subjects CTD patients. Brain donors had reduced compared with those donors. expression neural progenitor cell markers SOX2 PAX6 was derived organoids, while GSK3β, a key regulator...
A number of neurodegenerative disorders have been linked directly to the accumulation amyloid fibres. These fibres are made up proteins or peptides with altered structures and which join together in vivo association heparan sulphate-type polysaccharides.To examine most recent concepts biology sulphates their role aggregation peptide Abeta, tau protein, alpha-synuclein prions. The study also seeks analyse implications such as Alzheimer's Parkinson's disease prion diseases.In vitro, played an...
Abstract Creatine transporter deficiency (CTD) is an X-linked disease caused by mutations in the SLC6A8 gene. The impaired creatine uptake brain results intellectual disability, behavioral disorders, language delay, and seizures. In this work, we generated human organoids from induced pluripotent stem cells of healthy subjects CTD patients. Brain donors had reduced compared with those donors. expression neural progenitor cell markers SOX2 PAX6 was derived organoids, while GSK3β, a key...
Creatine transporter deficiency (CTD) is an X-linked disease caused by mutations in the SLC6A8 gene. The impaired creatine uptake brain results intellectual disability, behavioral disorders, language delay, and seizures. In this work, we generated human organoids from induced pluripotent stem cells of healthy subjects CTD patients. Brain donors had reduced compared with those donors. expression neural progenitor cell markers SOX2 PAX6 was derived organoids, while GSK3β, a key regulator...
Creatine transporter deficiency (CTD) is an X-linked disease caused by mutations in the SLC6A8 gene. The impaired creatine uptake brain results intellectual disability, behavioral disorders, language delay, and seizures. In this work, we generated human organoids from induced pluripotent stem cells of healthy subjects CTD patients. Brain donors had reduced compared with those donors. expression neural progenitor cell markers SOX2 PAX6 was CTD-derived organoids, while GSK3β, a key regulator...
Abstract Background Deposition of amyloid plaques and neurofibrillary tangles composed abnormally phosphorylated tau are the neuropathological hallmarks Alzheimer's disease (AD). However, years before accumulation protein aggregates, abnormal intraneuronal heparan sulfates (HS) is observed. This phenomenon breaks a dogma, since HS classically located on cell surface in extracellular matrix, leading to new autonomous concept tauopathy, which conceptual core FET‐OPEN ArrestAD 737390 project....