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4 results on '"Dauphinot, Luce"'

1. The lipid phosphatase Synaptojanin 1 undergoes a significant alteration in expression and solubility and is associated with brain lesions in Alzheimer’s disease.

Author

Ando, Kunie, Ndjim, Marième, Turbant, Sabrina, Fontaine, Gaëlle, Pregoni, Gustavo, Dauphinot, Luce, Suain, Valérie, Mansour, Salwa, Authelet, Michèle, De Decker, Robert, Delatour, Benoit, Brain Bank NeuroCEB Neuropathology Network, Duyckaerts, Charles, Leroy, Karelle, Potier, Marie-Claude, Brion, Jean Pierre, Ando, Kunie, Ndjim, Marième, Turbant, Sabrina, Fontaine, Gaëlle, Pregoni, Gustavo, Dauphinot, Luce, Suain, Valérie, Mansour, Salwa, Authelet, Michèle, De Decker, Robert, Delatour, Benoit, Brain Bank NeuroCEB Neuropathology Network, Duyckaerts, Charles, Leroy, Karelle, Potier, Marie-Claude, and Brion, Jean Pierre

Abstract

info:eu-repo/semantics/published

Published
2021

2. Increasing membrane cholesterol of neurons in culture recapitulates Alzheimer's disease early phenotypes

Author

Marquer, Catherine, Laine, Jeanne, Dauphinot, Luce, Hanbouch, Linda, Lemercier-Neuillet, Camille, Pierrot, Nathalie, Bossers, K., Le, Mickael, Corlier, Fabian, Benstaali, Caroline, Saudou, Frédéric, Thinakaran, Gopal, Cartier, Nathalie, Octave, Jean-Noël, Duyckaerts, Charles, Potier, Marie-Claude, Marquer, Catherine, Laine, Jeanne, Dauphinot, Luce, Hanbouch, Linda, Lemercier-Neuillet, Camille, Pierrot, Nathalie, Bossers, K., Le, Mickael, Corlier, Fabian, Benstaali, Caroline, Saudou, Frédéric, Thinakaran, Gopal, Cartier, Nathalie, Octave, Jean-Noël, Duyckaerts, Charles, and Potier, Marie-Claude

Published
2014

3. Increasing membrane cholesterol of neurons in culture recapitulates Alzheimer's disease early phenotypes.

Author

UCL - SSS/IONS/CEMO - Pôle Cellulaire et moléculaire, Marquer, Catherine, Laine, Jeanne, Dauphinot, Luce, Hanbouch, Linda, Lemercier-Neuillet, Camille, Pierrot, Nathalie, Bossers, Koen, Le, Mickael, Corlier, Fabian, Benstaali, Caroline, Saudou, Frédéric, Thinakaran, Gopal, Cartier, Nathalie, Octave, Jean-Noël, Duyckaerts, Charles, Potier, Marie-Claude, UCL - SSS/IONS/CEMO - Pôle Cellulaire et moléculaire, Marquer, Catherine, Laine, Jeanne, Dauphinot, Luce, Hanbouch, Linda, Lemercier-Neuillet, Camille, Pierrot, Nathalie, Bossers, Koen, Le, Mickael, Corlier, Fabian, Benstaali, Caroline, Saudou, Frédéric, Thinakaran, Gopal, Cartier, Nathalie, Octave, Jean-Noël, Duyckaerts, Charles, and Potier, Marie-Claude

Abstract

It is suspected that excess of brain cholesterol plays a role in Alzheimer's disease (AD). Membrane-associated cholesterol was shown to be increased in the brain of individuals with sporadic AD and to correlate with the severity of the disease. We hypothesized that an increase of membrane cholesterol could trigger sporadic AD early phenotypes.

Published
2014

4. Molecular signatures of cardiac defects in down syndrome lymphoblastoid cell lines suggest altered ciliome and hedgehog pathways

Author

UCL - (SLuc) Service de cardiologie pédiatrique, Ripoll, Clémentine, Rivals, Isabelle, Ait Yahya-Graison, Emilie, Dauphinot, Luce, Paly, Evelyne, Mircher, Clothilde, Ravel, Aimé, Grattau, Yann, Bléhaut, Henri, Mégarbane, André, DEMBOUR, Guy, de Fréminville, Bénédicte, Touraine, Renaud, Créau, Nicole, Potier, Marie Claude, Delabar, Jean Maurice, UCL - (SLuc) Service de cardiologie pédiatrique, Ripoll, Clémentine, Rivals, Isabelle, Ait Yahya-Graison, Emilie, Dauphinot, Luce, Paly, Evelyne, Mircher, Clothilde, Ravel, Aimé, Grattau, Yann, Bléhaut, Henri, Mégarbane, André, DEMBOUR, Guy, de Fréminville, Bénédicte, Touraine, Renaud, Créau, Nicole, Potier, Marie Claude, and Delabar, Jean Maurice

Abstract

Forty percent of people with Down syndrome exhibit heart defects, most often an atrioventricular septal defect (AVSD) and less frequently a ventricular septal defect (VSD) or atrial septal defect (ASD). Lymphoblastoid cell lines (LCLs) were established from lymphocytes of individuals with trisomy 21, the chromosomal abnormality causing Down syndrome. Gene expression profiles generated from DNA microarrays of LCLs from individuals without heart defects (CHD-; n = 22) were compared with those of LCLs from patients with cardiac malformations (CHD+; n = 21). After quantile normalization, principal component analysis revealed that AVSD carriers could be distinguished from a combined group of ASD or VSD (ASD+VSD) carriers. From 9,758 expressed genes, we identified 889 and 1,016 genes differentially expressed between CHD- and AVSD and CHD- and ASD+VSD, respectively, with only 119 genes in common. A specific chromosomal enrichment was found in each group of affected genes. Among the differentially expressed genes, more than 65% are expressed in human or mouse fetal heart tissues (GEO dataset). Additional LCLs from new groups of AVSD and ASD+VSD patients were analyzed by quantitative PCR; observed expression ratios were similar to microarray results. Analysis of GO categories revealed enrichment of genes from pathways regulating clathrin-mediated endocytosis in patients with AVSD and of genes involved in semaphorin-plexin-driven cardiogenesis and the formation of cytoplasmic microtubules in patients with ASD-VSD. A pathway-oriented search revealed enrichment in the ciliome for both groups and a specific enrichment in Hedgehog and Jak-stat pathways among ASD+VSD patients. These genes or related pathways are therefore potentially involved in normal cardiogenesis as well as in cardiac malformations observed in individuals with trisomy 21. © 2012 Ripoll et al.

Published
2012

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