J
Joseph A. Gogos
Researcher at Columbia University
Publications - 149
Citations - 17432
Joseph A. Gogos is an academic researcher from Columbia University. The author has contributed to research in topics: Catechol-O-methyl transferase & Schizophrenia. The author has an hindex of 67, co-authored 145 publications receiving 16040 citations. Previous affiliations of Joseph A. Gogos include Columbia University Medical Center & Howard Hughes Medical Institute.
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Convergent evidence for impaired AKT1-GSK3beta signaling in schizophrenia.
TL;DR: It is shown that haloperidol induces a stepwise increase in regulatory phosphorylation of AKT1 in the brains of treated mice that could compensate for an impaired function of this signaling pathway in schizophrenia.
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Catechol-O-methyltransferase-deficient mice exhibit sexually dimorphic changes in catecholamine levels and behavior
Joseph A. Gogos,Maria A. Morgan,Victoria N. Luine,Miklós Sántha,Sonoko Ogawa,Donald W. Pfaff,Maria Karayiorgou +6 more
TL;DR: The results provide conclusive evidence for an important sex- and region-specific contribution of COMT in the maintenance of steady-state levels of catecholamines in the brain and suggest a role for comT in some aspects of emotional and social behavior in mice.
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Strong association of de novo copy number mutations with sporadic schizophrenia.
TL;DR: The results suggest that rare de novo germline mutations contribute to schizophrenia vulnerability in sporadic cases and that rare genetic lesions at many different loci can account, at least in part, for the genetic heterogeneity of this disease.
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Impaired hippocampal–prefrontal synchrony in a genetic mouse model of schizophrenia
TL;DR: It is suggested that deficits in functional connectivity observed in patients with schizophrenia may be realized at the single-neuron level and impaired long-range synchrony of neural activity is one consequence of the 22q11.2 deletion.
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Altered brain microRNA biogenesis contributes to phenotypic deficits in a 22q11-deletion mouse model
Kimberly L. Stark,Bin Xu,Anindya Bagchi,Wen-Sung Lai,Hui Liu,Ruby Hsu,Xiang Wan,Paul Pavlidis,Alea A. Mills,Maria Karayiorgou,Joseph A. Gogos +10 more
TL;DR: Evidence is provided that the abnormal miRNA biogenesis emerges because of haploinsufficiency of the Dgcr8 gene, which encodes an RNA-binding moiety of the 'microprocessor' complex and contributes to the behavioral and neuronal deficits associated with the 22q11.2 microdeletion.