A5014671460- Neuroscience and Neuropharmacology Research
- Genetic Neurodegenerative Diseases
- Alzheimer's disease research and treatments
- Genetics and Neurodevelopmental Disorders
- Mitochondrial Function and Pathology
- RNA Research and Splicing
- Connexins and lens biology
- Biochemical effects in animals
- Diet and metabolism studies
- Cellular Mechanics and Interactions
- Molecular Biology Techniques and Applications
- Tryptophan and brain disorders
- Signaling Pathways in Disease
- Cultural Insights and Digital Impacts
- Dementia and Cognitive Impairment Research
- Neuroinflammation and Neurodegeneration Mechanisms
- Heat shock proteins research
- Cerebrospinal fluid and hydrocephalus
- Neuroscience of respiration and sleep
- Epigenetics and DNA Methylation
- Blood Pressure and Hypertension Studies
Collège de France
2018-2025
Université Paris Cité
2018-2024
Centre Interdisciplinaire de Recherche en Biologie
2018-2024
Centre National de la Recherche Scientifique
2018-2024
Inserm
2018-2024
Université Paris Sciences et Lettres
2018-2024
Sorbonne Paris Cité
2024
Institut Cochin
2018-2021
Délégation Paris 5
2018-2020
Institut de Psychiatrie et Neurosciences de Paris
2019
ABSTRACT Neurodevelopmental disorders, including X-linked intellectual disability, autism spectrum disorder or schizophrenia, can result from the mutation of oligophrenin-1 ( Ophn1 ), encoding a Rho-GTPase-activating protein. regulates synaptic development and function, in part via cytoskeleton reorganization, is expressed both neurons astrocytes. Despite crucial role astrocytes synapse altered neurodevelopmental their expression, specific impact astroglial deficiency on transmission...
Astrocytes undergo intense morphological maturation during development, changing from individual sparsely branched cells to polarized and tremendously ramified cells. Connexin 30, an astroglial gap-junction channel-forming protein expressed postnatally, regulates in situ the extension ramification of processes. However, involvement connexin 30 polarization, which is known control cell morphology, remains unexplored. We found that independently gap-junction-mediated intercellular biochemical...
Abstract Recent evidence showing degeneration of the noradrenergic system in locus coeruleus (LC) Alzheimer’s disease (AD) has motivated great interest noradrenaline (NA) as a potential brain hallmark disease. Despite current exploration blood markers for AD, deregulation plasma NA concentration ([NA] ) AD is currently not well understood. This retrospective study includes cohort 71 patients (32 patients, 22 with other dementia and 17 without dementia) who were given consultations memory...
Abstract During brain maturation, astrocytes establish complex morphologies unveiling intense structural plasticity. Connexin 30 (Cx30), a gap‐junction channel‐forming protein expressed postnatally, dynamically regulates during development astrocyte morphological properties by controlling ramification and extension of fine processes. However, the underlying mechanisms remain unexplored. Here, we found in vitro that Cx30 interacts with actin cytoskeleton inhibits its reorganization dynamics...
Abstract Brain dysfunction in myotonic dystrophy type 1 (DM1), the prototype of toxic RNA disorders, has been mainly attributed to neuronal misprocessing, while little attention given non-neuronal brain cells. Here, using a transgenic mouse model DM1 that expresses mutant various cell types (neurons, astroglia, and oligodendroglia), we demonstrate astrocytes exhibit impaired ramification polarization vivo defects adhesion, spreading, migration. RNA-dependent toxicity phenotypes are also...
Abstract Astrocytes are involved in several aspects of neuronal development and properties which altered intellectual disability (ID). Oligophrenin‐1 is a RhoGAP protein implicated actin cytoskeleton regulation, whose mutations associated with X‐linked ID. expressed neurons, where its functions have been widely reported at the synapse, as well glial cells. However, roles astrocytes still largely unexplored. Using vitro vivo models oligophrenin1 disruption astrocytes, we found that regulates...
Abstract Brain dysfunction in myotonic dystrophy type 1 (DM1), the prototype of toxic RNA disorders, has been mainly attributed to neuronal misprocessing, while little attention given non-neuronal brain cells. Using a transgenic mouse model DM1 that expresses mutant various cell types, we demonstrate astrocytes exhibit impaired ramification and polarization vivo defects adhesion, spreading migration. RNA-dependent toxicity phenotypes was also found human transfected glial In line with...