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1. DIAPH3 predicts survival of patients with MGMT-methylated glioblastoma

Author

Chehade, Georges, El Hajj, Nady, Aittaleb, Mohamed, Alkailani, Maisa I., Bejaoui, Yosra, Mahdi, Asma, Aldaalis, Arwa A. H., Verbiest, Michael, Lelotte, Julie, Ruiz-Reig, Nuria, Dura, Irene, Raftopoulos, Christian, Tajeddine, Nicolas, Tissir, Fadel, Chehade, Georges, El Hajj, Nady, Aittaleb, Mohamed, Alkailani, Maisa I., Bejaoui, Yosra, Mahdi, Asma, Aldaalis, Arwa A. H., Verbiest, Michael, Lelotte, Julie, Ruiz-Reig, Nuria, Dura, Irene, Raftopoulos, Christian, Tajeddine, Nicolas, and Tissir, Fadel

Abstract

Background: Glioblastoma is one of the most aggressive primary brain tumors, with a poor outcome despite multimodal treatment. Methylation of the MGMT promoter, which predicts the response to temozolomide, is a well-established prognostic marker for glioblastoma. However, a difference in survival can still be detected within the MGMT methylated group, with some patients exhibiting a shorter survival than others, emphasizing the need for additional predictive factors. Methods: We analyzed DIAPH3 expression in glioblastoma samples from the cancer genome atlas (TCGA). We also retrospectively analyzed one hundred seventeen histological glioblastomas from patients operated on at Saint-Luc University Hospital between May 2013 and August 2019. We analyzed the DIAPH3 expression, explored the relationship between mRNA levels and Patient's survival after the surgical resection. Finally, we assessed the methylation pattern of the DIAPH3 promoter using a targeted deep bisulfite sequencing approach. Results: We found that 36% and 1% of the TCGA glioblastoma samples exhibit copy number alterations and mutations in DIAPH3, respectively. We scrutinized the expression of DIAPH3 at single cell level and detected an overlap with MKI67 expression in glioblastoma proliferating cells, including neural progenitor-like, oligodendrocyte progenitor-like and astrocyte-like states. We quantitatively analyzed DIAPH3 expression in our cohort and uncovered a positive correlation between DIAPH3 mRNA level and patient's survival. The effect of DIAPH3 was prominent in MGMT-methylated glioblastoma. Finally, we report that the expression of DIAPH3 is at least partially regulated by the methylation of three CpG sites in the promoter region. Conclusion: We propose that combining the DIAPH3 expression with MGMT methylation could offer a better prediction of survival and more adapted postsurgical treatment for patients with MGMT-methylated glioblastoma.

Published
2024

2. Chromatin establishes an immature version of neuronal protocadherin selection during the naive-to-primed conversion of pluripotent stem cells.

Author

Almenar-Queralt, Angels, Almenar-Queralt, Angels, Merkurjev, Daria, Kim, Hong Sook, Navarro, Michael, Ma, Qi, Chaves, Rodrigo S, Allegue, Catarina, Driscoll, Shawn P, Chen, Andrew G, Kohlnhofer, Bridget, Fong, Lauren K, Woodruff, Grace, Mackintosh, Carlos, Bohaciakova, Dasa, Hruska-Plochan, Marian, Tadokoro, Takahiro, Young, Jessica E, El Hajj, Nady, Dittrich, Marcus, Marsala, Martin, Goldstein, Lawrence SB, Garcia-Bassets, Ivan, Almenar-Queralt, Angels, Almenar-Queralt, Angels, Merkurjev, Daria, Kim, Hong Sook, Navarro, Michael, Ma, Qi, Chaves, Rodrigo S, Allegue, Catarina, Driscoll, Shawn P, Chen, Andrew G, Kohlnhofer, Bridget, Fong, Lauren K, Woodruff, Grace, Mackintosh, Carlos, Bohaciakova, Dasa, Hruska-Plochan, Marian, Tadokoro, Takahiro, Young, Jessica E, El Hajj, Nady, Dittrich, Marcus, Marsala, Martin, Goldstein, Lawrence SB, and Garcia-Bassets, Ivan

Abstract

In the mammalian genome, the clustered protocadherin (cPCDH) locus provides a paradigm for stochastic gene expression with the potential to generate a unique cPCDH combination in every neuron. Here we report a chromatin-based mechanism that emerges during the transition from the naive to the primed states of cell pluripotency and reduces, by orders of magnitude, the combinatorial potential in the human cPCDH locus. This mechanism selectively increases the frequency of stochastic selection of a small subset of cPCDH genes after neuronal differentiation in monolayers, 10-month-old cortical organoids and engrafted cells in the spinal cords of rats. Signs of these frequent selections can be observed in the brain throughout fetal development and disappear after birth, except in conditions of delayed maturation such as Down's syndrome. We therefore propose that a pattern of limited cPCDH-gene expression diversity is maintained while human neurons still retain fetal-like levels of maturation.

Published
2019

3. Methylomic profiling in trisomy 21 identifies cognition- and Alzheimer's disease-related dysregulation

Author

Haertle, Larissa, Mueller, Tobias, Lardenoije, Roy, Maierhofer, Anna, Dittrich, Marcus, Riemens, Renzo J. M., Stora, Samantha, Roche, Mathilde, Leber, Markus, Riedel-Heller, Steffi, Wagner, Michael, Scherer, Martin, Ravel, Aime, Mircher, Clotilde, Cieuta-Walti, Cecile, Durand, Sophie, van de Hove, Daniel L. A., Hoffmann, Per, Ramirez, Alfredo, Haaf, Thomas, El Hajj, Nady, Megarbane, Andre, Haertle, Larissa, Mueller, Tobias, Lardenoije, Roy, Maierhofer, Anna, Dittrich, Marcus, Riemens, Renzo J. M., Stora, Samantha, Roche, Mathilde, Leber, Markus, Riedel-Heller, Steffi, Wagner, Michael, Scherer, Martin, Ravel, Aime, Mircher, Clotilde, Cieuta-Walti, Cecile, Durand, Sophie, van de Hove, Daniel L. A., Hoffmann, Per, Ramirez, Alfredo, Haaf, Thomas, El Hajj, Nady, and Megarbane, Andre

Abstract

Background: Trisomy 21 (T21) is associated with intellectual disability that ranges from mild to profound with an average intellectual quotient of around 50. Furthermore, T21 patients have a high risk of developing Alzheimer's disease (AD) early in life, characterized by the presence of senile plaques of amyloid protein and neurofibrillary tangles, leading to neuronal loss and cognitive decline. We postulate that epigenetic factors contribute to the observed variability in intellectual disability, as well as at the level of neurodegeneration seen in T21 individuals. Materials and Methods: A genome-wide DNA methylation study was performed using Illumina Infinium (R) MethylationEPIC BeadChips on whole blood DNA of 3 male T21 patients with low IQ, 8 T21 patients with high IQ (4 males and 4 females), and 21 age- and sex-matched control samples (12 males and 9 females) in order to determine whether DNA methylation alterations could help explain variation in cognitive impairment between individuals with T21. In view of the increased risk of developing AD in T21 individuals, we additionally investigated the T21-associated sites in published blood DNA methylation data from the AgeCoDe cohort (German study on Ageing, Cognition, and Dementia). AgeCoDe represents a prospective longitudinal study including non-demented individuals at baseline of which a part develops AD dementia at follow-up. Results: Two thousand seven hundred sixteen differentially methylated sites and regions discriminating T21 and healthy individuals were identified. In the T21 high and low IQ comparison, a single CpG located in the promoter of PELI1 was differentially methylated after multiple testing adjustment. For the same contrast, 69 differentially methylated regions were identified. Performing a targeted association analysis for the significant T21-associated CpG sites in the AgeCoDe cohort, we found that 9 showed significant methylation differences related to AD dementia, including one in the ADAM10

Published
2019

4. Chromatin establishes an immature version of neuronal protocadherin selection during the naive-to-primed conversion of pluripotent stem cells.

Author

Almenar-Queralt, Angels, Almenar-Queralt, Angels, Merkurjev, Daria, Kim, Hong Sook, Navarro, Michael, Ma, Qi, Chaves, Rodrigo S, Allegue, Catarina, Driscoll, Shawn P, Chen, Andrew G, Kohlnhofer, Bridget, Fong, Lauren K, Woodruff, Grace, Mackintosh, Carlos, Bohaciakova, Dasa, Hruska-Plochan, Marian, Tadokoro, Takahiro, Young, Jessica E, El Hajj, Nady, Dittrich, Marcus, Marsala, Martin, Goldstein, Lawrence SB, Garcia-Bassets, Ivan, Almenar-Queralt, Angels, Almenar-Queralt, Angels, Merkurjev, Daria, Kim, Hong Sook, Navarro, Michael, Ma, Qi, Chaves, Rodrigo S, Allegue, Catarina, Driscoll, Shawn P, Chen, Andrew G, Kohlnhofer, Bridget, Fong, Lauren K, Woodruff, Grace, Mackintosh, Carlos, Bohaciakova, Dasa, Hruska-Plochan, Marian, Tadokoro, Takahiro, Young, Jessica E, El Hajj, Nady, Dittrich, Marcus, Marsala, Martin, Goldstein, Lawrence SB, and Garcia-Bassets, Ivan

Abstract

In the mammalian genome, the clustered protocadherin (cPCDH) locus provides a paradigm for stochastic gene expression with the potential to generate a unique cPCDH combination in every neuron. Here we report a chromatin-based mechanism that emerges during the transition from the naive to the primed states of cell pluripotency and reduces, by orders of magnitude, the combinatorial potential in the human cPCDH locus. This mechanism selectively increases the frequency of stochastic selection of a small subset of cPCDH genes after neuronal differentiation in monolayers, 10-month-old cortical organoids and engrafted cells in the spinal cords of rats. Signs of these frequent selections can be observed in the brain throughout fetal development and disappear after birth, except in conditions of delayed maturation such as Down's syndrome. We therefore propose that a pattern of limited cPCDH-gene expression diversity is maintained while human neurons still retain fetal-like levels of maturation.

Published
2019

5. Methylomic profiling in trisomy 21 identifies cognition- and Alzheimer's disease-related dysregulation

Author

Haertle, Larissa, Mueller, Tobias, Lardenoije, Roy, Maierhofer, Anna, Dittrich, Marcus, Riemens, Renzo J. M., Stora, Samantha, Roche, Mathilde, Leber, Markus, Riedel-Heller, Steffi, Wagner, Michael, Scherer, Martin, Ravel, Aime, Mircher, Clotilde, Cieuta-Walti, Cecile, Durand, Sophie, van de Hove, Daniel L. A., Hoffmann, Per, Ramirez, Alfredo, Haaf, Thomas, El Hajj, Nady, Megarbane, Andre, Haertle, Larissa, Mueller, Tobias, Lardenoije, Roy, Maierhofer, Anna, Dittrich, Marcus, Riemens, Renzo J. M., Stora, Samantha, Roche, Mathilde, Leber, Markus, Riedel-Heller, Steffi, Wagner, Michael, Scherer, Martin, Ravel, Aime, Mircher, Clotilde, Cieuta-Walti, Cecile, Durand, Sophie, van de Hove, Daniel L. A., Hoffmann, Per, Ramirez, Alfredo, Haaf, Thomas, El Hajj, Nady, and Megarbane, Andre

Abstract

Background: Trisomy 21 (T21) is associated with intellectual disability that ranges from mild to profound with an average intellectual quotient of around 50. Furthermore, T21 patients have a high risk of developing Alzheimer's disease (AD) early in life, characterized by the presence of senile plaques of amyloid protein and neurofibrillary tangles, leading to neuronal loss and cognitive decline. We postulate that epigenetic factors contribute to the observed variability in intellectual disability, as well as at the level of neurodegeneration seen in T21 individuals. Materials and Methods: A genome-wide DNA methylation study was performed using Illumina Infinium (R) MethylationEPIC BeadChips on whole blood DNA of 3 male T21 patients with low IQ, 8 T21 patients with high IQ (4 males and 4 females), and 21 age- and sex-matched control samples (12 males and 9 females) in order to determine whether DNA methylation alterations could help explain variation in cognitive impairment between individuals with T21. In view of the increased risk of developing AD in T21 individuals, we additionally investigated the T21-associated sites in published blood DNA methylation data from the AgeCoDe cohort (German study on Ageing, Cognition, and Dementia). AgeCoDe represents a prospective longitudinal study including non-demented individuals at baseline of which a part develops AD dementia at follow-up. Results: Two thousand seven hundred sixteen differentially methylated sites and regions discriminating T21 and healthy individuals were identified. In the T21 high and low IQ comparison, a single CpG located in the promoter of PELI1 was differentially methylated after multiple testing adjustment. For the same contrast, 69 differentially methylated regions were identified. Performing a targeted association analysis for the significant T21-associated CpG sites in the AgeCoDe cohort, we found that 9 showed significant methylation differences related to AD dementia, including one in the ADAM10

Published
2019

6. 183-P

Author

Khalaf, Roy A., Rayes, Roni, Ghasham, Mona, El Hajj, Nady, Sabbagh, Amira S., Mahfouz, Rami A., Khalaf, Roy A., Rayes, Roni, Ghasham, Mona, El Hajj, Nady, Sabbagh, Amira S., and Mahfouz, Rami A.

Abstract

Aim: This study represents the first report on KIR distribution among patients with Familial Mediterranean Fever (FMF). Samples and Methods: We studied 56 unrelated Lebanese FMF patients, had their DNA typed using Sequence Specific Primer (SSP) technique for the presence of 16 KIR gene and pseudogene loci and compared them to the general Lebanese population. Results: In addition to sharing common features with the general population, we the AA genotype was still the most frequent; however, with six new KIR profiles identified. Conclusions: There was no statistically significant distribution of the different KIR genes between the cases (FMF patients) and controls (Lebanese population); however, an increase in the BB genotype was noted leading to an interesting future research question of whether or not KIR genotype is involved in the predisposition to or pathogenesis of FMF. This is the first report that describes the KIR genotypic profile in this important clinical disease.

Published
2018

7. Natural Killer Cell Immunoglobulin-like Receptor (KIR) genotypes in Follicular Lymphoma patients

Author

Khalaf, Roy, Hoteit, Rouba, Yazbek, Soha, El Hajj, Nady, Otrock, Zaher, Khansa, Sarah, Sabbagh, Amira, Shammaa, Dina, Mahfouz, Rami, Khalaf, Roy, Hoteit, Rouba, Yazbek, Soha, El Hajj, Nady, Otrock, Zaher, Khansa, Sarah, Sabbagh, Amira, Shammaa, Dina, and Mahfouz, Rami

Abstract

Aims The Natural Killer Cell Immunoglobulin-like Receptor (KIR) genotype profiling in Follicular Lymphoma has not been reported before in the literature. Materials and methods DNA extracted from 20 Follicular Lymphoma patients and 62 healthy controls was analyzed for KIR genotyping using a polymerase chain reaction/sequence specific primers technique (PCR/SSP) for the presence of 16 KIR gene and pseudogene loci. Results The AA, AB, and BB genotype frequencies were, respectively, 20%, 60% and 20% with an A:B ratio of 1:1. KIR 2DL4, KIR 3DL2, KIR 3DL3, and KIR 3DP1*003 were presented in all individuals. No significant difference between patients and controls was detected. Conclusion KIR genotyping profile does not seem to be associated with Follicular Lymphoma. The results presented in this pilot research represent the first international report about this important clinical entity. Abbreviations KIR, Killer Cell Immunoglobulin-like Receptors; PCR, Polymerase chain reaction; SSP, Sequence specific primers; NHL, Non-Hodgkin's lymphoma; Ig, Immunoglobulin; FL, Follicular Lymphoma; NK, Natural killer; HLA, Human leukocyte antigens; MHC, Major histocompatibility complex; ITIM, Immunoreceptor tyrosine based inhibition motifs; HSTCL, Hepatosplenic T-cell lymphoma; UV, Ultraviolet

Published
2016

8. Killer Cell Immunoglobulin-Like Receptor (KIR) Genotypes in Patients with Recurrent Tonsillitis

Author

Khalaf, Roy, Bitar, Mohamad, Shamseddeen, Wael, El Hajj, Nady, Ibrahim, Georges, Greige, Layal, Zaatari, Ghazi, Khalaf, Roy, Bitar, Mohamad, Shamseddeen, Wael, El Hajj, Nady, Ibrahim, Georges, Greige, Layal, and Zaatari, Ghazi

Abstract

Aims: This study represents the first report on the distribution of killer cell immunoglobulin-like receptor (KIR) genotype among recurrent tonsillitis patients. We recruited 34 Lebanese pediatric patients diagnosed with recurrent tonsillitis and had their DNA typed using sequence-specific primer technique for the presence of 16 KIR loci. Results: We observed that 25 different KIR genotypes were present similar to the general control population with the same KIR gene content. There was no statistically significant difference in the distribution of the activating and inhibitory KIR genes between the two categories. Like in the general control population, we noted a predominance of the AB genotype; however, the KIR genotypic distribution among the tonsillitis patients was much more heterogeneous with even new genotypes not reported in the control group. Conclusions: Although the sample size is small, this first study observes an interesting heterogeneous KIR gene profile in recurrent tonsillitis that warrants larger and further research in the area for the true biological and clinical significance of this observation.

Published
2016

9. De novo mutations in HCN1 cause early infantile epileptic encephalopathy

Author

May, Patrick [collaborator], Balling, Rudi [collaborator], Barisic, Nina [collaborator], Baulac, Stéphanie [collaborator], Caglayan, Hande S. [collaborator], Craiu, Dana C. [collaborator], De Jonghe, Peter [collaborator], Depienne, Christel [collaborator], Gormley, Padhraig [collaborator], Guerrini, Renzo [collaborator], Helbig, Ingo [collaborator], Hjalgrim, Helle [collaborator], Hoffman-Zacharska, Dorota [collaborator], Jähn, Johanna [collaborator], Klein, Karl Martin [collaborator], Koeleman, Bobby P. C. [collaborator], Komarek, Vladimir [collaborator], Krause, Roland [collaborator], LeGuern, Eric [collaborator], Lehesjoki, Anna-Elina [collaborator], Lemke, Johannes R. [collaborator], Lerche, Holger [collaborator], Marini, Carla [collaborator], Møller, Rikke S. [collaborator], Muhle, Hiltrud [collaborator], Palotie, Aarno [collaborator], Pal, Deb [collaborator], Rosenow, Felix [collaborator], Selmer, Kaja [collaborator], Serratosa, José M. [collaborator], Sisodiya, Sanjay [collaborator], Stephani, Ulrich [collaborator], Sterbova, Katalin [collaborator], Striano, Pasquale [collaborator], Suls, Arvid [collaborator], Talvik, Tiina [collaborator], von Spiczak, Sarah [collaborator], Weber, Yvonne [collaborator], Weckhuysen, Sarah [collaborator], Zara, Federico [collaborator], Luxembourg Centre for Systems Biomedicine (LCSB): Experimental Neurobiology (Balling Group) [research center], Nava, Caroline, Dalle, Carine, Rastetter, Agnès, Striano, Pasquale, de Kovel, Carolien G. F., Nabbout, Rima, Cancès, Claude, Ville, Dorothée, Brilstra, Eva H., Gobbi, Giuseppe, Raffo, Emmanuel, Bouteiller, Delphine, Marie, Yannick, Trouillard, Oriane, Robbiano, Angela, Keren, Boris, Agher, Dahbia, Roze, Emmanuel, Lesage, Suzanne, Nicolas, Aude, Brice, Alexis, Baulac, Michel, Vogt, Cornelia, El Hajj, Nady, Schneider, Eberhard, Suls, Arvid, Weckhuysen, Sarah, Gormley, Padhraig, Lehesjoki, Anna-Elina, De Jonghe, Peter, Helbig, Ingo, Baulac, Stephanie, Zara, Federico, Koeleman, Bobby P. C., Consortium, Euroepinomics R. E. S., Haaf, Thomas, LeGuern, Eric, Depienne, Christel, May, Patrick [collaborator], Balling, Rudi [collaborator], Barisic, Nina [collaborator], Baulac, Stéphanie [collaborator], Caglayan, Hande S. [collaborator], Craiu, Dana C. [collaborator], De Jonghe, Peter [collaborator], Depienne, Christel [collaborator], Gormley, Padhraig [collaborator], Guerrini, Renzo [collaborator], Helbig, Ingo [collaborator], Hjalgrim, Helle [collaborator], Hoffman-Zacharska, Dorota [collaborator], Jähn, Johanna [collaborator], Klein, Karl Martin [collaborator], Koeleman, Bobby P. C. [collaborator], Komarek, Vladimir [collaborator], Krause, Roland [collaborator], LeGuern, Eric [collaborator], Lehesjoki, Anna-Elina [collaborator], Lemke, Johannes R. [collaborator], Lerche, Holger [collaborator], Marini, Carla [collaborator], Møller, Rikke S. [collaborator], Muhle, Hiltrud [collaborator], Palotie, Aarno [collaborator], Pal, Deb [collaborator], Rosenow, Felix [collaborator], Selmer, Kaja [collaborator], Serratosa, José M. [collaborator], Sisodiya, Sanjay [collaborator], Stephani, Ulrich [collaborator], Sterbova, Katalin [collaborator], Striano, Pasquale [collaborator], Suls, Arvid [collaborator], Talvik, Tiina [collaborator], von Spiczak, Sarah [collaborator], Weber, Yvonne [collaborator], Weckhuysen, Sarah [collaborator], Zara, Federico [collaborator], Luxembourg Centre for Systems Biomedicine (LCSB): Experimental Neurobiology (Balling Group) [research center], Nava, Caroline, Dalle, Carine, Rastetter, Agnès, Striano, Pasquale, de Kovel, Carolien G. F., Nabbout, Rima, Cancès, Claude, Ville, Dorothée, Brilstra, Eva H., Gobbi, Giuseppe, Raffo, Emmanuel, Bouteiller, Delphine, Marie, Yannick, Trouillard, Oriane, Robbiano, Angela, Keren, Boris, Agher, Dahbia, Roze, Emmanuel, Lesage, Suzanne, Nicolas, Aude, Brice, Alexis, Baulac, Michel, Vogt, Cornelia, El Hajj, Nady, Schneider, Eberhard, Suls, Arvid, Weckhuysen, Sarah, Gormley, Padhraig, Lehesjoki, Anna-Elina, De Jonghe, Peter, Helbig, Ingo, Baulac, Stephanie, Zara, Federico, Koeleman, Bobby P. C., Consortium, Euroepinomics R. E. S., Haaf, Thomas, LeGuern, Eric, and Depienne, Christel

Published
2014

10. De novo mutations in HCN1 cause early infantile epileptic encephalopathy

Author

May, Patrick [collaborator], Balling, Rudi [collaborator], Barisic, Nina [collaborator], Baulac, Stéphanie [collaborator], Caglayan, Hande S. [collaborator], Craiu, Dana C. [collaborator], De Jonghe, Peter [collaborator], Depienne, Christel [collaborator], Gormley, Padhraig [collaborator], Guerrini, Renzo [collaborator], Helbig, Ingo [collaborator], Hjalgrim, Helle [collaborator], Hoffman-Zacharska, Dorota [collaborator], Jähn, Johanna [collaborator], Klein, Karl Martin [collaborator], Koeleman, Bobby P. C. [collaborator], Komarek, Vladimir [collaborator], Krause, Roland [collaborator], LeGuern, Eric [collaborator], Lehesjoki, Anna-Elina [collaborator], Lemke, Johannes R. [collaborator], Lerche, Holger [collaborator], Marini, Carla [collaborator], Møller, Rikke S. [collaborator], Muhle, Hiltrud [collaborator], Palotie, Aarno [collaborator], Pal, Deb [collaborator], Rosenow, Felix [collaborator], Selmer, Kaja [collaborator], Serratosa, José M. [collaborator], Sisodiya, Sanjay [collaborator], Stephani, Ulrich [collaborator], Sterbova, Katalin [collaborator], Striano, Pasquale [collaborator], Suls, Arvid [collaborator], Talvik, Tiina [collaborator], von Spiczak, Sarah [collaborator], Weber, Yvonne [collaborator], Weckhuysen, Sarah [collaborator], Zara, Federico [collaborator], Luxembourg Centre for Systems Biomedicine (LCSB): Experimental Neurobiology (Balling Group) [research center], Nava, Caroline, Dalle, Carine, Rastetter, Agnès, Striano, Pasquale, de Kovel, Carolien G. F., Nabbout, Rima, Cancès, Claude, Ville, Dorothée, Brilstra, Eva H., Gobbi, Giuseppe, Raffo, Emmanuel, Bouteiller, Delphine, Marie, Yannick, Trouillard, Oriane, Robbiano, Angela, Keren, Boris, Agher, Dahbia, Roze, Emmanuel, Lesage, Suzanne, Nicolas, Aude, Brice, Alexis, Baulac, Michel, Vogt, Cornelia, El Hajj, Nady, Schneider, Eberhard, Suls, Arvid, Weckhuysen, Sarah, Gormley, Padhraig, Lehesjoki, Anna-Elina, De Jonghe, Peter, Helbig, Ingo, Baulac, Stephanie, Zara, Federico, Koeleman, Bobby P. C., Consortium, Euroepinomics R. E. S., Haaf, Thomas, LeGuern, Eric, Depienne, Christel, May, Patrick [collaborator], Balling, Rudi [collaborator], Barisic, Nina [collaborator], Baulac, Stéphanie [collaborator], Caglayan, Hande S. [collaborator], Craiu, Dana C. [collaborator], De Jonghe, Peter [collaborator], Depienne, Christel [collaborator], Gormley, Padhraig [collaborator], Guerrini, Renzo [collaborator], Helbig, Ingo [collaborator], Hjalgrim, Helle [collaborator], Hoffman-Zacharska, Dorota [collaborator], Jähn, Johanna [collaborator], Klein, Karl Martin [collaborator], Koeleman, Bobby P. C. [collaborator], Komarek, Vladimir [collaborator], Krause, Roland [collaborator], LeGuern, Eric [collaborator], Lehesjoki, Anna-Elina [collaborator], Lemke, Johannes R. [collaborator], Lerche, Holger [collaborator], Marini, Carla [collaborator], Møller, Rikke S. [collaborator], Muhle, Hiltrud [collaborator], Palotie, Aarno [collaborator], Pal, Deb [collaborator], Rosenow, Felix [collaborator], Selmer, Kaja [collaborator], Serratosa, José M. [collaborator], Sisodiya, Sanjay [collaborator], Stephani, Ulrich [collaborator], Sterbova, Katalin [collaborator], Striano, Pasquale [collaborator], Suls, Arvid [collaborator], Talvik, Tiina [collaborator], von Spiczak, Sarah [collaborator], Weber, Yvonne [collaborator], Weckhuysen, Sarah [collaborator], Zara, Federico [collaborator], Luxembourg Centre for Systems Biomedicine (LCSB): Experimental Neurobiology (Balling Group) [research center], Nava, Caroline, Dalle, Carine, Rastetter, Agnès, Striano, Pasquale, de Kovel, Carolien G. F., Nabbout, Rima, Cancès, Claude, Ville, Dorothée, Brilstra, Eva H., Gobbi, Giuseppe, Raffo, Emmanuel, Bouteiller, Delphine, Marie, Yannick, Trouillard, Oriane, Robbiano, Angela, Keren, Boris, Agher, Dahbia, Roze, Emmanuel, Lesage, Suzanne, Nicolas, Aude, Brice, Alexis, Baulac, Michel, Vogt, Cornelia, El Hajj, Nady, Schneider, Eberhard, Suls, Arvid, Weckhuysen, Sarah, Gormley, Padhraig, Lehesjoki, Anna-Elina, De Jonghe, Peter, Helbig, Ingo, Baulac, Stephanie, Zara, Federico, Koeleman, Bobby P. C., Consortium, Euroepinomics R. E. S., Haaf, Thomas, LeGuern, Eric, and Depienne, Christel

Published
2014

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