V des Portes

CHU de Lyon - Hôpital Femme-Mère-Enfant, Lyons, Rhône-Alpes, France

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Publications (127)510.76 Total impact

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    ABSTRACT: Mutations of the CDKL5 gene cause early epileptic encephalopathy. Patients manifest refractory epilepsy, beginning before the age of 3 months, which is associated with severe psychomotor delay and features that overlap with Rett syndrome. We report here a patient with mosaicism for CDKL5 exonic deletion, with the presence of two mutant alleles. The affected 4-year-old girl presented with infantile spasms, beginning at the age of 9 months, but subsequent progression of the disease was consistent with the classical CDKL5-related phenotype. A deletion of exons 17 and 18 was suspected on the basis of Multiplex Ligation Probe Amplification analysis, but unexpected results for cDNA analysis, which showed the presence of an abnormal transcript with the deletion of exon 18 only, led us to suspect that two distinct events might have occurred. We used custom array-CGH to determine the size and breakpoints of these deletions. Exon 18 was deleted from one of the abnormal alleles, and exon 17 was deleted from the other. A Fork Stalling and Template Switching (FoSTeS) mechanism was proposed to explain the two events, given the presence of regions of microhomology at the breakpoints. We propose here an original involvement of the FoSTeS mechanism to explain the co-occurrence of these two events in the CDKL5 gene in a single patient. This patient highlights the difficulties involved in the detection of such abnormalities, particularly when they occur in a mosaic state and involve two distinct mutational events in a single gene. © 2014 Wiley Periodicals, Inc.
    American Journal of Medical Genetics Part A 04/2014; · 2.30 Impact Factor
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    ABSTRACT: The c.429_452dup24 of the ARX gene is a rare genetic anomaly, leading to X-Linked Intellectual Disability without brain malformation. While in certain cases c.429_452dup24 has been associated with specific clinical patterns such as Partington syndrome, the consequence of this mutation has been also often classified as "non-specific Intellectual Disability". The present work aims at a more precise description of the clinical features linked to the c.429_452dup24 mutation. We clinically reviewed all affected patients identified in France over a five-year period, i.e. 27 patients from 12 different families. Detailed cognitive, behavioural, and motor evaluation, as well as standardized videotaped assessments of oro-lingual and gestural praxis, were performed. In a sub-group of 13 ARX patients, kinematic and MRI studies were further accomplished to better characterize the motor impairment prevalent in the ARX patients group. To ensure that data were specific to the ARX gene mutation and did not result from low-cognitive functioning per se, a group of 27 age- and IQ-matched Down syndrome patients served as control. Neuropsychological and motor assessment indicated that the c.429_452dup24 mutation constitutes a recognizable clinical syndrome: ARX patients exhibiting Intellectual Disability, without primary motor impairment, but with a very specific upper limb distal motor apraxia associated with a pathognomonic hand-grip. Patients affected with the so-called Partington syndrome, which involves major hand dystonia and orolingual apraxia, exhibit the most severe symptoms of the disorder. The particular "reach and grip" impairment which was observed in all ARX patients, but not in Down syndrome patients, was further characterized by the kinematic data: (i) loss of preference for the index finger when gripping an object, (ii) major impairment of fourth finger deftness, and (iii) a lack of pronation movements. This lack of distal movement coordination exhibited by ARX patients is associated with the loss of independent digital dexterity and is similar to the distortion of individual finger movements and posture observed in Limb Kinetic Apraxia. These findings suggest that the ARX c.429_452dup24 mutation may be a developmental model for Limb Kinetic Apraxia.
    Orphanet Journal of Rare Diseases 02/2014; 9(1):25. · 4.32 Impact Factor
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    ABSTRACT: The present paper investigates the clinical picture and the different clinical signs that reveal pineal region tumors or appear during the course of the follow-up. Biological malignancy and tumor extension determine the semiology and its setting up mode. Typical endocrine signs, dominated by abnormal puberty development, are frequently a part of the clinical scene. Bifocal or ectopic localization in the hypothalamic-pituitary region is accompanied by other endocrine signs such as ante- or post-pituitary insufficiencies which occur several months or even years after the first neurological signs appear. Due to a mass syndrome and obstructive hydrocephalus, intracranial hypertension signs are frequent but unspecific. A careful ophthalmologic examination is essential to search upward gaze paralysis and other signs of the Parinaud's tetrad or pentad. Midbrain dysfunction, including extrinsic aqueduct stenosis, are also prevalent. Except for abnormal pubertal signs, hyper-melatoninemia (secretory tumors) or a-hypo-melatoninemia (tumors destructing pineal) generally remains dormant. Some patients present sleep problems such as narcolepsy or sleepiness during the daytime as well as behavioral problems. This suggests a hypothalamic extension rather than a true consequence of melatonin secretion anomalies. Similarly, some patients may present signs of a "pinealectomized" syndrome, including (cluster) headaches, tiredness, eventually responsive to melatonin.
    Neurochirurgie 01/2014; · 0.32 Impact Factor
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    ABSTRACT: The strong positive-allometric relationship between brain size, cortical extension and gyrification complexity, recently highlighted in the general population, could be modified by brain developmental disorders. Indeed, in case of brain growth insufficiency, the pathophysiological relevance of the “simplified gyral pattern” phenotype is strongly disputed since almost no genotype–phenotype correlations have been found in primary microcephalies. Using surface scaling analysis and newly-developed spectral analysis of gyrification (Spangy), we tested whether the gyral simplification in groups of severe microcephalies related to ASPM, PQBP1 or fetal-alcohol-syndrome could be fully explained by brain size reduction according to the allometric scaling law established in typically-developing control groups, or whether an additional disease effect was to be suspected. We found the surface area reductions to be fully explained by scaling effect, leading to predictable folding intensities measured by gyrification indices. As for folding pattern assessed by spectral analysis, scaling effect also accounted for the majority of the variations, but an additional negative or positive disease effect was found in the case of ASPM and PQBP1-linked microcephalies, respectively. Our results point out the necessity of taking allometric scaling into account when studying the gyrification variability in pathological conditions. They also show that the quantitative analysis of gyrification complexity through spectral analysis can enable distinguishing between even (predictable, non-specific) and uneven (unpredictable, maybe disease-specific) gyral simplifications.
    NeuroImage 01/2014; 102:317–331. · 6.25 Impact Factor
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    ABSTRACT: To identify the aetiology of patients with infantile spasms and propose practical guidelines for diagnostic strategies. We performed a retrospective study of children with West syndrome. Prenatal and birth medical history, characteristics of epilepsy, psychomotor development, biological and genetic screening, and aetiology were reported. Brain MRI was performed at least once and was repeated after two years of age if no aetiology was identified. Eighty children were included. Aetiology was identified in 40 children: 17 with acquired cause (seven with stroke and six with hypoxic-ischaemic encephalopathy) and 23 with developmental pathology (seven with tuberous sclerosis, eight with cerebral malformations, and eight with various genetic abnormalities). The yield of brain imaging was high, providing a diagnosis for 32 patients. Two subtle brain lesions were detected only after two years of age, based on subsequent MRI. Genetic testing provided a diagnosis for the remaining eight patients. Although this is a retrospective study, the results provide a basis to review the aetiology of infantile spasms and confirm the role of cerebral MRI in first-line diagnosis. Cases with a genetic aetiology have been diagnosed with increasing frequency due to better diagnostic capabilities. We propose guidelines for a practical diagnostic approach and discuss the relevant use of genetics in the future.
    European journal of paediatric neurology: EJPN: official journal of the European Paediatric Neurology Society 11/2013; · 2.01 Impact Factor
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    ABSTRACT: Advances in understanding the underlying mechanisms of conditions such as fragile X syndrome (FXS) and autism spectrum disorders have revealed heterogeneous populations. Recent trials of novel FXS therapies have highlighted several challenges including subpopulations with possibly differential therapeutic responses, the lack of specific outcome measures capturing the full range of improvements of patients with FXS, and a lack of biomarkers that can track whether a specific mechanism is responsive to a new drug and whether the response correlates with clinical improvement. We review the phenotypic heterogeneity of FXS and the implications for clinical research in FXS and other neurodevelopmental disorders. Residual levels of fragile X mental retardation protein (FMRP) expression explain in part the heterogeneity in the FXS phenotype; studies indicate a correlation with both cognitive and behavioral deficits. However, this does not fully explain the extent of phenotypic variance observed or the variability of drug response. Post hoc analyses of studies involving the selective mGluR5 antagonist mavoglurant and the GABAB agonist arbaclofen have uncovered significant therapeutic responses following patient stratification according to FMR1 promoter methylation patterns or baseline severity of social withdrawal, respectively. Future studies designed to quantify disease modification will need to develop new strategies to track changes effectively over time and in multiple symptom domains. Appropriate selection of patients and outcome measures is central to optimizing future clinical investigations of these complex disorders.
    Psychopharmacology 10/2013; · 4.06 Impact Factor
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    ABSTRACT: Successful non-verbal social interaction between human beings requires dynamic and efficient encoding of others' gestures. Our study aimed at identifying neural markers of social interaction and goal variations in a non-verbal task. For this, we recorded simultaneously the electroencephalogram from two participants (dual-EEG), an actor and an observer, and their arm/hand kinematics in a real face-to-face paradigm. The observer watched "biological actions" performed by the human actor and "non-biological actions" performed by a robot. All actions occurred within an interactive or non-interactive context depending on whether the observer had to perform a complementary action or not (e.g., the actor presents a saucer and the observer either places the corresponding cup or does nothing). We analysed the EEG signals of both participants (i.e., beta (~20Hz) oscillations as an index of cortical motor activity and motor related potentials (MRPs)). We identified markers of social interactions by synchronising EEG to the onset of the actor's movement. Movement kinematics did not differ in the two context conditions and the MRPs of the actor were similar in the two conditions. For the observer, however, an observation-related MRP was measured in all conditions but was more negative in the interactive context over fronto-central electrodes. Moreover, this feature was specific to biological actions. Concurrently, the suppression of beta oscillations was observed in the actor's EEG and the observer's EEG rapidly after the onset of the actor's movement. Critically, this suppression was stronger in the interactive than in the non-interactive context despite the fact that movement kinematics did not differ in the two context conditions. For the observer, this modulation was observed independently of whether the actor was a human or a robot. Our results suggest that acting in a social context induced analogous modulations of motor and sensorimotor regions in observer and actor. Sharing a common goal during an interaction seems thus to evoke a common representation of the global action that includes both actor and observer movements.
    Neuropsychologia 10/2013; · 3.48 Impact Factor
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    ABSTRACT: Kawasaki disease is an acute and time-limited systemic vasculitis primarily affecting young children. We describe an 18-month-old girl with Kawasaki disease who developed cerebral infarction following complete occlusion of her right internal carotid artery. The occlusion occurred 10 days after the onset of fever, while she was on high-dose aspirin, and the day after she received intravenous immunoglobulin treatment. We present the first literature review on this very rare complication. Stroke is a rare neurological complication in Kawasaki disease. Optimal treatment should be begun as soon as possible after diagnosis. Intravenous immunoglobulins seem to reduce the cerebrovascular complications, but evaluation of hydration status is strongly recommended before performing such treatment.
    Pediatric Neurology 10/2013; · 1.42 Impact Factor
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    ABSTRACT: Creatine and guanidinoacetate are biomarkers of creatine metabolism. Their assays in body fluids may be used for detecting patients with primary creatine deficiency disorders (PCDD), a class of inherited diseases. Their laboratory values in blood and urine may vary with age, requiring that reference normal values are given within the age range. Despite the long known role of creatine for muscle physiology, muscle signs are not necessarily the major complaint expressed by PCDD patients. These disorders drastically affect brain function inducing, in patients, intellectual disability, autistic behavior and other neurological signs (delays in speech and language, epilepsy, ataxia, dystonia and choreoathetosis), being a common feature the drop in brain creatine content. For this reason, screening of PCDD patients has been repeatedly carried out in populations with neurological signs. This report is aimed at providing reference laboratory values and related age ranges found for a large scale population of patients with neurological signs (more than 6 thousand patients) previously serving as a background population for screening French patients with PCDD. These reference laboratory values and age ranges compare rather favorably with literature values for healthy populations. Some differences are also observed, and female participants are discriminated from male participants as regards to urine but not blood values including creatine on creatinine ratio and guanidinoacetate on creatinine ratio values. Such gender differences were previously observed in healthy populations; they might be explained by literature differential effects of testosterone and estrogen in adolescents and adults, and by estrogen effects in prepubertal age on SLC6A8 function. Finally, though they were acquired on a population with neurological signs, the present data might reasonably serve as reference laboratory values in any future medical study exploring abnormalities of creatine metabolism and transport.
    Molecular Genetics and Metabolism 09/2013; · 2.83 Impact Factor
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    ABSTRACT: FG syndrome, Lujan syndrome, and Ohdo syndrome, the Maat-Kievit-Brunner type, have been described as distinct syndromes with overlapping non-specific features and different missense mutations of the MED12 gene have been reported in all of them. We report a family including 10 males and 1 female affected with profound non-specific intellectual disability (ID) which was linked to a 30-cM region extending from Xp11.21 (ALAS2) to Xq22.3 (COL4A5). Parallel sequencing of all X-chromosome exons identified a frameshift mutation (c.5898dupC) of MED12. Mutated mRNA was not affected by non-sense mediated RNA decay and induced an additional abnormal isoform due to activation of cryptic splice-sites in exon 41. Dysmorphic features common to most affected males were long narrow face, high forehead, flat malar area, high nasal bridge, and short philtrum. Language was absent or very limited. Most patients had a friendly personality. Cognitive impairment, varying from borderline to profound ID was similarly observed in seven heterozygous females. There was no correlation between cognitive function and X-chromosome inactivation profiles in blood cells. The severe degree of ID in male patients, as well as variable cognitive impairment in heterozygous females suggests that the duplication observed in the present family may have a more severe effect on MED12 function than missense mutations. In a cognitively impaired male from this family, who also presented with tall stature and dysmorphism and did not have the MED12 mutation, a 600-kb duplication at 17p13.3 including the YWHAE gene, was found in a mosaic state. © 2013 Wiley Periodicals, Inc.
    American Journal of Medical Genetics Part A 08/2013; · 2.30 Impact Factor
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    ABSTRACT: Evidence that the motor and the linguistic systems share common syntactic representations would open new perspectives on language evolution. Here, crossing disciplinary boundaries, we explore potential parallels between the structure of simple actions and that of sentences. First, examining Typically Developing (TD) children displacing a bottle with or without knowledge of its weight prior to movement onset, we provide kinematic evidence that the sub-phases of this displacing action (reaching + moving the bottle) manifest a structure akin to linguistic embedded dependencies. Then, using the same motor task, we reveal that children suffering from specific language impairment (SLI), whose core deficit affects syntactic embedding and dependencies, manifest specific structural motor anomalies parallel to their linguistic deficits. In contrast to TD children, SLI children performed the displacing-action as if its sub-phases were juxtaposed rather than embedded. The specificity of SLI’s structural motor deficit was confirmed by testing an additional control group: Fragile-X Syndrome patients, whose language capacity, though delayed, comparatively spares embedded dependencies, displayed slower but structurally normal motor performances. By identifying the presence of structural representations and dependency computations in the motor system and by showing their selective deficit in SLI patients, these findings point to a potential motor origin for language syntax.
    PLoS ONE 08/2013; · 3.53 Impact Factor
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    ABSTRACT: Pyridoxine-dependent epilepsy (PDE) is a rare autosomal recessive metabolic disease. A delay of treatment may affect outcome and early initiation of pyridoxine based on effective diagnosis is crucial to ensure good cognitive outcome in neonates. A consensus for the diagnosis of PDE is based on refractive seizures and responsiveness to pyridoxine, however, a growing body of evidence suggests that additional elements should be considered which include biochemical data, genetic screening, and EEG monitoring. We present a case study of a neonate with PDE, who presented with misleading clinical presentation and a novel mutation in the antiquitin (ALDH7A1) gene (A294V), and highlight important aspects in order to consider the definition of diagnosis and management of PDE in the light of more recent data.
    European journal of paediatric neurology: EJPN: official journal of the European Paediatric Neurology Society 07/2013; · 2.01 Impact Factor
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    ABSTRACT: OBJECTIVE: To illustrate the significance of distortion of the interhemispheric fissure (DIHF) associated with impacted medial borders of the frontal lobes and discuss the relevance of DIHF in prenatal diagnosis. METHODS: A retrospective observational study of 13 foetuses, in which DIHF was identified on prenatal imaging, was conducted to investigate associated biological and anatomical anomalies. RESULTS: Anatomical anomalies associated with DIHF were identified in 10 cases including mainly midline anomalies (syntelencephaly [n=2], lobar holoprosencephaly [n=1], Aicardi syndrome [n=2],), but also schizencephaly (n=1), cortical dysplasia (n=1) and more complex cerebral malformations [n=3], including neural tube defect in 2 cases. Chromosomal anomaly was identified in 2 cases, including 6p deletion in a case without associated CNS anomalies and a complex mosaicism in a case with synthelencephaly. In two prenatal cases, the finding was isolated based on both pre and post-natal imaging resulting in healthy individuals. CONCLUSION: Presence of DIHF on prenatal imaging may provide a clue for diagnosis of cerebral anomalies, especially those involving the midline. If DIHF is "isolated" based on prenatal ultrasound, MRI is recommended for careful analysis of gyration and midline, especially optic and olfactory structures. Karyotyping is also recommended to look for chromosomal anomalies.
    Ultrasound in Obstetrics and Gynecology 05/2013; · 3.56 Impact Factor
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    ABSTRACT: Action observation and execution share overlapping neural resonating mechanisms. In the present study, we sought to examine the effect of the activation of this system during concurrent movement observation and execution in a prehension task, when no a priori information about the requirements of grasping action was available. Although it is known that simultaneous activation by observation and execution influences motor performance, the importance of the delays of these two events and the specific effect of movement observation itself (and not the prediction of the to-be-observed movement) on action performance are poorly known. Fine-grained kinematic analysis of both the transport and grasp components of the movement should provide knowledge about the influence of movement observation on the precision and the performance of the executed movement. The experiment involved two real participants who were asked to grasp a different side of a single object that was composed of a large and a small part. In the first experiment, we measured how the transport component and the grasp component were affected by movement observation. We tested whether this influence was greater if the observed movement occurred just before the onset of movement (200 ms) or well before the onset of movement (1 s). In a second experiment, to reproduce the previous experiment and to verify the specificity of the grasping movements, we also included a condition consisting of pointing towards the object. Both experiments showed two main results. A general facilitation of the transport component was found when observing a simultaneous action, independent of its congruency. Moreover, a specific facilitation of the grasp component was present during the observation of a congruent action when movement execution and observation were nearly synchronised. While the general facilitation may arise from a competition between the two participants as they reached for the object, the specific facilitation of the grasp component seems to be directly related to mirror neuron system activity induced by action observation itself. Moreover, the time course of the events appears to be an essential factor for this modulation, implying the transitory activation of the mirror neuron system.
    Experimental Brain Research 04/2013; · 2.22 Impact Factor
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    ABSTRACT: The genetic causes of malformations of cortical development (MCD) remain largely unknown. Here we report the discovery of multiple pathogenic missense mutations in TUBG1, DYNC1H1 and KIF2A, as well as a single germline mosaic mutation in KIF5C, in subjects with MCD. We found a frequent recurrence of mutations in DYNC1H1, implying that this gene is a major locus for unexplained MCD. We further show that the mutations in KIF5C, KIF2A and DYNC1H1 affect ATP hydrolysis, productive protein folding and microtubule binding, respectively. In addition, we show that suppression of mouse Tubg1 expression in vivo interferes with proper neuronal migration, whereas expression of altered γ-tubulin proteins in Saccharomyces cerevisiae disrupts normal microtubule behavior. Our data reinforce the importance of centrosomal and microtubule-related proteins in cortical development and strongly suggest that microtubule-dependent mitotic and postmitotic processes are major contributors to the pathogenesis of MCD.
    Nature Genetics 04/2013; · 35.21 Impact Factor
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    ABSTRACT: SLC16A2, the gene for the 2(nd) member of the solute carrier family 16 (monocarboxylic acid transporter), located on chromosome Xq13.2, encodes a very efficient thyroid hormone (TH) transporter: monocarboxylate transporter 8, MCT8. Its loss of function is responsible in males for a continuum of psychomotor retardation ranging from severe (no motor acquisition, no speech) to mild (ability to walk with help and a few words of speech). Triiodothyronine uptake measurement in transfected cells and, more recently, patient fibroblasts, has been described to study the functional consequences of MCT8 mutations. Here we describe 3 novel MCT8 mutations, including one missense variation not clearly predicted to be damaging but found in a severely affected patient. Functional studies in fibroblasts and JEG3 cells demonstrate the usefulness of both cellular models in validating the deleterious effects of a new MCT8 mutation if there is still a doubt as to its pathogenicity. Moreover, the screening of fibroblasts from a large number of patient fibroblasts and of transfected mutations has allowed us to demonstrate that JEG3 transfected cells are more relevant than fibroblasts in revealing a genotype-phenotype correlation.
    Human Mutation 04/2013; · 5.21 Impact Factor
  • Archives de Pédiatrie. 04/2013; 20(4):430–431.
  • Archives de Pédiatrie. 04/2013; 20(4):425.
  • Archives de Pédiatrie. 04/2013; 20(4):427–428.
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    ABSTRACT: We report the case of a 33-year-old pregnant woman. The third-trimester ultrasound scan during pregnancy revealed fetal bilateral ventricular dilatation, macrosomia and a transverse diameter of the cerebellum at the 30th centile. A brain MRI scan at 31 weeks of gestation led to a diagnosis of hypoplasia of the cerebellar vermis without hemisphere abnormalities and a non compressive expansion of the cisterna magna. The fetal karyotype was 46,XX. The pregnancy was terminated and array-CGH analysis of the fetus identified a 238 kb de novo deletion on chromosome Xp12, encompassing part of OPHN1 gene. Further studies revealed a completely skewed pattern of X inactivation. OPHN1 is involved in X-linked mental retardation (XLMR) with cerebellar hypoplasia and encodes a Rho-GTPase-activating protein called oligophrenin-1, which is produced throughout the developing mouse brain and in the hippocampus and Purkinje cells of the cerebellum in adult mice. Neuropathological examination of the female fetus revealed cerebellar hypoplasia and the heterotopia of Purkinje cells at multiple sites in the white matter of the cerebellum. This condition mostly affects male fetuses in humans. We report here the first case of a de novo partial deletion of OPHN1, with radiological and neuropathological examination, in a female fetus.
    European journal of medical genetics 02/2013; · 1.57 Impact Factor

Publication Stats

2k Citations
510.76 Total Impact Points


  • 2006–2014
    • CHU de Lyon - Hôpital Femme-Mère-Enfant
      Lyons, Rhône-Alpes, France
  • 2004–2014
    • HCL
      Noida, Uttar Pradesh, India
  • 2011–2013
    • University Hospital of Lausanne
      • Service de génétique médicale
      Lausanne, Vaud, Switzerland
  • 2006–2013
    • French National Centre for Scientific Research
      • • Laboratoire sur le langage, le cerveau et la cognition (L2C2)
      • • Institut des sciences cognitives
      Lyon, Rhone-Alpes, France
  • 2005–2013
    • Université René Descartes - Paris 5
      • Faculté de Médecine
      Lutetia Parisorum, Île-de-France, France
    • St. Vincent Hospital
      Green Bay, Wisconsin, United States
  • 2012
    • Hôpital Universitaire Robert Debré
      • Département de Génétique
      Lutetia Parisorum, Île-de-France, France
  • 2006–2012
    • Claude Bernard University Lyon 1
      Villeurbanne, Rhône-Alpes, France
  • 2004–2012
    • Hospices Civils de Lyon
      Lyons, Rhône-Alpes, France
  • 2010
    • University of Lyon
      Lyons, Rhône-Alpes, France
    • Assistance Publique – Hôpitaux de Paris
      Lutetia Parisorum, Île-de-France, France
  • 2008
    • Centre Hospitalier Universitaire de Lyon
      Lyons, Rhône-Alpes, France
  • 2007
    • Institut Cochin
      Lutetia Parisorum, Île-de-France, France
    • CHU de Lyon - Hôpital de la Croix-Rousse
      Lyons, Rhône-Alpes, France
  • 2004–2005
    • Centre Hospitalier Lyon Sud
      Lyons, Rhône-Alpes, France
  • 2003
    • University of California, Davis
      Davis, California, United States
  • 2000–2003
    • Unité Inserm U1077
      Caen, Lower Normandy, France
    • French Institute of Health and Medical Research
      Lutetia Parisorum, Île-de-France, France
    • Ospedale Pediatrico Bambino Gesù
      Roma, Latium, Italy
  • 2000–2002
    • Hôpital Saint-Vincent-de-Paul – Hôpitaux universitaires Paris Centre
      Lutetia Parisorum, Île-de-France, France
  • 1996–2000
    • Institut de Génétique Moléculaire de Montpellier
      Montpelhièr, Languedoc-Roussillon, France
  • 1999
    • Hôpital Charles-Nicolle
      Tunis-Ville, Tūnis, Tunisia