BACKGROUND: Pediatric bipolar I disorder (BP-I) and childhood schizophrenia (SZ) share certain symptoms (e.g., psychosis, aggression/irritability [A/I]), and the psychotic and A/I features are treated with neuroleptics in both disorders. Thus, it is of interest to examine the association of GAD1 to child BP-I because of its recently reported association to childhood SZ. METHODS: Child BP-I probands were obtained by consecutive new case ascertainment, and the phenotype was defined as current DSM-IV BP-I (manic or mixed phase) with at least one of the cardinal symptoms of mania (i.e., elation and/or grandiosity) and a Children's Global Assessment Scale score < or =60 (clinical impairment). These child BP-I probands are part of a large, ongoing, longitudinal study in which the phenotype has been validated by unique symptoms, longitudinal stability, and 7-8 times greater family loading than adult BP-I probands. Genotyping was performed using a TaqMan Validated SNP Genotyping Assay, and FBAT was used for analysis. RESULTS: There were 48 families. The rs2241165 A allele was preferentially transmitted (FBAT chi(2) = 5.2, df = 1, p = 0.022). No interaction between this GAD1 SNP and the Val66 BDNF allele was found. CONCLUSIONS: These data are consistent with some shared genetic vulnerability between child BP-I and SZ, which may be related to similar treatments.
BACKGROUND: Pediatric bipolar I disorder (BP-I) and childhood schizophrenia (SZ) share certain symptoms (e.g., psychosis, aggression/irritability [A/I]), and the psychotic and A/I features are treated with neuroleptics in both disorders. Thus, it is of interest to examine the association of GAD1 to child BP-I because of its recently reported association to childhood SZ. METHODS:Child BP-I probands were obtained by consecutive new case ascertainment, and the phenotype was defined as current DSM-IV BP-I (manic or mixed phase) with at least one of the cardinal symptoms of mania (i.e., elation and/or grandiosity) and a Children's Global Assessment Scale score < or =60 (clinical impairment). These child BP-I probands are part of a large, ongoing, longitudinal study in which the phenotype has been validated by unique symptoms, longitudinal stability, and 7-8 times greater family loading than adult BP-I probands. Genotyping was performed using a TaqMan Validated SNP Genotyping Assay, and FBAT was used for analysis. RESULTS: There were 48 families. The rs2241165 A allele was preferentially transmitted (FBAT chi(2) = 5.2, df = 1, p = 0.022). No interaction between this GAD1 SNP and the Val66 BDNF allele was found. CONCLUSIONS: These data are consistent with some shared genetic vulnerability between childBP-I and SZ, which may be related to similar treatments.
Authors: Stefano Marenco; Antonina A Savostyanova; Jan Willem van der Veen; Matthew Geramita; Alexa Stern; Alan S Barnett; Bhaskar Kolachana; Eugenia Radulescu; Fengyu Zhang; Joseph H Callicott; Richard E Straub; Jun Shen; Daniel R Weinberger Journal: Neuropsychopharmacology Date: 2010-03-31 Impact factor: 7.853
Authors: Heike Weber; Claus Jürgen Scholz; Katharina Domschke; Christian Baumann; Benedikt Klauke; Christian P Jacob; Wolfgang Maier; Jürgen Fritze; Borwin Bandelow; Peter Michael Zwanzger; Thomas Lang; Lydia Fehm; Andreas Ströhle; Alfons Hamm; Alexander L Gerlach; Georg W Alpers; Tilo Kircher; Hans-Ulrich Wittchen; Volker Arolt; Paul Pauli; Jürgen Deckert; Andreas Reif Journal: PLoS One Date: 2012-05-25 Impact factor: 3.240
Authors: Benjamin I Goldstein; Boris Birmaher; Gabrielle A Carlson; Melissa P DelBello; Robert L Findling; Mary Fristad; Robert A Kowatch; David J Miklowitz; Fabiano G Nery; Guillermo Perez-Algorta; Anna Van Meter; Cristian P Zeni; Christoph U Correll; Hyo-Won Kim; Janet Wozniak; Kiki D Chang; Manon Hillegers; Eric A Youngstrom Journal: Bipolar Disord Date: 2017-09-25 Impact factor: 6.744