المؤلفون: Pritchard, Antonia, Clair, David St, Lemmon, Helen, Mann, David M.A, Lendon, Corinne

المصدر: Neuroscience Letters ; volume 366, issue 2, page 126-129 ; ISSN 0304-3940

مصطلحات موضوعية: General Neuroscience

الإتاحة: https://doi.org/10.1016/j.neulet.2004.05.023Test
https://api.elsevier.com/content/article/PII:S0304394004006032?httpAccept=text/xmlTest
https://api.elsevier.com/content/article/PII:S0304394004006032?httpAccept=text/plainTest

المؤلفون: Hannon, Eilis, Dempster, Emma, Viana, Joana, Burrage, Joe, Smith, Adam R., Macdonald, Ruby, Clair, David St, Mustard, Colette, Breen, Gerome, Therman, Sebastian, Kaprio, Jaakko, Timothea Toulopoulou, Hulshoff Pol, Hilleke E., Bohlken, Marc M., Kahn, Rene S., Nenadic, Igor, Hultman, Christina M., Murray, Robin M., Collier, David A., Bass, Nick

المصدر: Genome Biology; 8/30/2016, Vol. 17, p1-16, 16p

المؤلفون: Harris, Judith M., Coates, John, Cummings, Alastair M., Craddock, Nick J., Clair, David St., Lendon, Corinne L.

المصدر: Neurobiology of Aging ; volume 21, page 174-175 ; ISSN 0197-4580

مصطلحات موضوعية: Geriatrics and Gerontology, Developmental Biology, Neurology (clinical), Aging, General Neuroscience

الإتاحة: https://doi.org/10.1016/s0197-4580Test(00)82123-5
https://api.elsevier.com/content/article/PII:S0197458000821235?httpAccept=text/xmlTest
https://api.elsevier.com/content/article/PII:S0197458000821235?httpAccept=text/plainTest

المؤلفون: Blackwood, Douglas, Clair, David St., Muir, Walter

المصدر: European Archives of Psychiatry and Clinical Neuroscience ; volume 240, issue 3, page 191-196 ; ISSN 0175-758X 1433-8491

مصطلحات موضوعية: Pharmacology (medical), Biological Psychiatry, Psychiatry and Mental health, General Medicine, Neuropsychology and Physiological Psychology, General Neuroscience

الإتاحة: https://doi.org/10.1007/bf02190763Test

المؤلفون: Goodwin, Guy M., Chiswick, Ann, Egan, Vincent, Clair, David St., Brettle, Ray P.

المصدر: Aids ; volume 4, issue 12, page 1243-1250 ; ISSN 0269-9370

الإتاحة: https://doi.org/10.1097/00002030-199012000-00010Test
http://journals.lww.com/00002030-199012000-00010Test

المؤلفون: Scott, Dianne, de Jesus, Carolina Maria, Clair, David St.

المصدر: Agenda ; issue 8, page 71 ; ISSN 1013-0950

مصطلحات موضوعية: Literature and Literary Theory

الإتاحة: https://doi.org/10.2307/4065638Test

المؤلفون: Nithianantharajah, Jess, Komiyama, Noboru H, McKechanie, Andrew, Johnstone, Mandy, Blackwood, Douglas H, Clair, David St, Emes, Richard D, van de Lagemaat, Louie N, Saksida, Lisa M, Bussey, Timothy J, Grant, Seth G N

المصدر: Nature Neuroscience; Jan2013, Vol. 16 Issue 1, p16-24, 9p, 2 Diagrams, 4 Graphs

مصطلحات موضوعية: VERTEBRATES, ANIMAL cognition, GENOMES, GENES, ANIMAL psychopathology

مستخلص: The origins and evolution of higher cognitive functions, including complex forms of learning, attention and executive functions, are unknown. A potential mechanism driving the evolution of vertebrate cognition early in the vertebrate lineage (550 million years ago) was genome duplication and subsequent diversification of postsynaptic genes. Here we report, to our knowledge, the first genetic analysis of a vertebrate gene family in cognitive functions measured using computerized touchscreens. Comparison of mice carrying mutations in each of the four Dlg paralogs showed that simple associative learning required Dlg4, whereas Dlg2 and Dlg3 diversified to have opposing functions in complex cognitive processes. Exploiting the translational utility of touchscreens in humans and mice, testing Dlg2 mutations in both species showed that Dlg2's role in complex learning, cognitive flexibility and attention has been highly conserved over 100 million years. Dlg-family mutations underlie psychiatric disorders, suggesting that genome evolution expanded the complexity of vertebrate cognition at the cost of susceptibility to mental illness. [ABSTRACT FROM AUTHOR]

: Copyright of Nature Neuroscience is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

المؤلفون: Thorleifsson, Gudmar, Walters, G. Bragi, Hewitt, Alex W., Masson, Gisli, Helgason, Agnar, DeWan, Andrew, Sigurdsson, Asgeir, Jonasdottir, Adalbjorg, Gudjonsson, Sigurjon A., Magnusson, Kristinn P., Stefansson, Hreinn, Lam, Dennis S. C., Tam, Pancy O. S., Gudmundsdottir, Gudrun J., Southgate, Laura, Burdon, Kathryn P., Gottfredsdottir, Maria Soffia, Aldred, Micheala A., Mitchell, Paul, Clair, David St.

المصدر: Nature Genetics; Oct2010, Vol. 42 Issue 10, p906-909, 4p, 1 Chart, 1 Graph

مصطلحات موضوعية: GLAUCOMA, RETINAL ganglion cells, LOCUS (Genetics), GENETIC mutation, DISEASE susceptibility, ELECTROCARDIOGRAPHY, ATRIAL fibrillation, GENETICS

مستخلص: We conducted a genome-wide association study for primary open-angle glaucoma (POAG) in 1,263 affected individuals (cases) and 34,877 controls from Iceland. We identified a common sequence variant at 7q31 (rs4236601[A], odds ratio (OR) = 1.36, P = 5.0 × 10⁻¹⁰). We then replicated the association in sample sets of 2,175 POAG cases and 2,064 controls from Sweden, the UK and Australia (combined OR = 1.18, P = 0.0015) and in 299 POAG cases and 580 unaffected controls from Hong Kong and Shantou, China (combined OR = 5.42, P = 0.0021). The risk variant identified here is located close to CAV1 and CAV2, both of which are expressed in the trabecular meshwork and retinal ganglion cells that are involved in the pathogenesis of POAG. [ABSTRACT FROM AUTHOR]

: Copyright of Nature Genetics is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

المؤلفون: Sanbing Shen, Bing Lang, Nakamoto, Chizu, Feng Zhang, Jin Pu, Soh-Leh Kuan, Chatzi, Christina, Shuisheng He, Mackie, Iain, Brandon, Nicholas J., Marquis, Karen L., Day, Mark, Hurko, Orest, McCaig, Colin D., Riedel, Gernot, Clair, David St.

المصدر: Journal of Neuroscience; 10/22/2008, Vol. 28 Issue 43, p10893-10904, 12p, 1 Chart, 10 Graphs

مصطلحات موضوعية: SCHIZOPHRENIA, PHENOTYPES, BACTERIAL artificial chromosomes, PREFRONTAL cortex, LABORATORY mice

مستخلص: Disrupted-in-Schizophrenia-1 (DISC1), identified by positional cloning of a balanced translocation (1;11) with the breakpoint in intron 8 of a large Scottish pedigree, is associated with a range of neuropsychiatric disorders including schizophrenia. To model this mutation in mice, we have generated Disc1tr transgenic mice expressing 2 copies of truncated Disc1 encoding the first 8 exons using a bacterial artificial chromosome (BAC). With this partial simulation of the human situation, we have discovered a range of phenotypes including a series of novel features not previously reported. Disc1tr transgenic mice display enlarged lateral ventricles, reduced cerebral cortex, partial agenesis of the corpus callosum, and thinning of layers II/III with reduced neural proliferation at midneurogenesis. Parvalbumin GABAergic neurons are reduced in the hippocampus and medial prefrontal cortex, and displaced in the dorsolateral frontal cortex. In culture, transgenic neurons grow fewer and shorter neurites. Behaviorally, transgenic mice exhibit increased immobility and reduced vocalization in depression-related tests, and impairment in conditioning of latent inhibition. These abnormalities in Disc1tr transgenic mice are consistent with findings in severe schizophrenia. [ABSTRACT FROM AUTHOR]

: Copyright of Journal of Neuroscience is the property of Society for Neuroscience and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

المؤلفون: Breen, Gerome, Harwood, Adrian J, Gregory, Kathryn, Sinclair, Maggie, Collier, David, Clair, David St, Williams, Robin SB

المصدر: Bipolar Disorders; Apr2004, Vol. 6 Issue 2, p156-161, 6p

مصطلحات موضوعية: MENTAL illness treatment, BIPOLAR disorder, SCHIZOPHRENIA, LITHIUM, VALPROIC acid, CARBAMAZEPINE, PEPTIDASE, ENZYMES, BLOOD plasma

مستخلص: Breen G, Harwood AJ, Gregory K, Sinclair M, Collier D, St Clair D, Williams RSB. Two peptidase activities decrease in treated bipolar disorder not schizophrenic patients. Bipolar Disord 2004: 6: 156–161. © Blackwell Munksgaard, 2004 Inhibition of prolyl oligopeptidase (PO) in primary neuronal cultures has been shown to reverse the effect of the common mood-stabilizers lithium, valproic acid and carbamazepine. In clinical studies, abnormal plasma PO activity has been associated with bipolar disorder (BD) and schizophrenia. However, this association is complicated by the discovery in bovine plasma of a Z-Pro-prolinal-insensitive peptidase (ZIP), a novel enzyme that cleaves the same substrate as PO. We developed an assay to distinguish between ZIP and PO and measured both activities in plasma from 48 BD and 50 schizophrenic patients undergoing treatment and compared them with 50 control subjects. ZIP activity is restricted to blood plasma, whereas PO activity is present in the cytosol of lymphocytes, but can also be detected in blood plasma. Significant decreases in their plasma activities were found between treated BD (p = 0.007 and 0.03 respectively) but not schizophrenic (p > 0.05) patients and controls. We have found that the enzyme activity previously reported as plasma PO actually comprises two enzymes, PO and ZIP. This study shows a statistically significant decrease of both enzymes in BD patients undergoing lithium treatment. No statistically significant change in PO or ZIP activity is observed in schizophrenic patients. [ABSTRACT FROM AUTHOR]

: Copyright of Bipolar Disorders is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)