期刊论文详细信息
BMC Psychiatry
Antipsychotic medications and cognitive functioning in bipolar disorder: moderating effects of COMT Val108/158 Met genotype
Jim van Os2  Marjan Drukker3  Claudia JP Simons1  Baer Arts3 
[1] GGZE, Institute for Mental Health Care Eindhoven en de Kempen, P.O. Box 909, Eindhoven, AX, 5600, The Netherlands;King’s College London, King’s Health Partners, Department of Psychosis Studies, Institute of Psychiatry, London, United Kingdom;Department of Psychiatry and Psychology, School for Mental Health and Neuroscience, European Graduate School of Neuroscience (EURON), South Limburg Mental Health Research and Teaching Network (SEARCH), Maastricht University Medical Centre, P.O. Box 616 (DRT 12), Maastricht, MD, 6200, The Netherlands
关键词: COMT;    Antipsychotics;    Cognition;    Bipolar disorder;   
Others  :  1124130
DOI  :  10.1186/1471-244X-13-63
 received in 2012-06-06, accepted in 2013-02-08,  发布年份 2013
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【 摘 要 】

Background

There is a negative association between the use of antipsychotics and cognitive functioning in bipolar patients, which may be mediated by altered dopamine signaling in selected brain areas, and moderation thereof by genetic sequence variation such as COMT Val108/158Met. The interaction between antipsychotic drug use and the COMT Val108/158Met genotype on two-year cognitive functioning in bipolar patients was examined.

Methods

Interaction between the COMT Val108/158Met and antipsychotics on a composite cognitive measure was examined in 51 bipolar patients who were assessed 12 times at two-monthly intervals over a period of two years (379 observations).

Results

There was a significant negative effect of the interaction between antipsychotic medications and Val allele load on the composite cognitive measure in bipolar patients (p < 0.001).

Conclusions

The negative effects of antipsychotics on cognitive functioning in bipolar disorder may be moderated by the COMT Val 108/158 Met genotype, with a negative effect of Val allele load. If replicated, the results may be indicative of pharmacogenetic interactions in bipolar disorder.

【 授权许可】

   
2013 Arts et al; licensee BioMed Central Ltd.

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【 参考文献 】
  • [1]Arts B, Jabben N, Krabbendam L, Van Os J: Meta-analyses of cognitive functioning in euthymic bipolar patients and their first-degree relatives. Psychol Med 2008, 38(6):771-785.
  • [2]Bora E, Yucel M, Pantelis C: Cognitive endophenotypes of bipolar disorder: A meta-analysis of neuropsychological deficits in euthymic patients and their first-degree relatives. J Affect Disord 2009, 113:1-20.
  • [3]Kurtz MM, Gerraty RT: A meta-analytic investigation of neurocognitive deficits in bipolar illness: profile and effects of clinical state. Neuropsychology 2009, 23(5):551-562.
  • [4]Mann-Wrobel MC, Carreno JT, Dickinson D: Meta-analysis of neuropsychological functioning in euthymic bipolar disorder: an update and investigation of moderator variables. Bipolar Disord 2011, 13(4):334-342.
  • [5]Balanza-Martinez V, Selva G, Martinez-Aran A, Prickaerts J, Salazar J, Gonzalez-Pinto A, Vieta E, Tabares-Seisdedos R: Neurocognition in bipolar disorders–a closer look at comorbidities and medications. Eur J Pharmacol 2010, 626(1):87-96.
  • [6]Jamrozinski K, Gruber O, Kemmer C, Falkai P, Scherk H: Neurocognitive functions in euthymic bipolar patients. Acta Psychiatr Scand 2009, 119(5):365-374.
  • [7]Torrent C, Martinez-Aran A, Daban C, Amann B, Balanza-Martinez V, Del Mar BC, Cruz N, Franco C, Tabares-Seisdedos R, Vieta E: Effects of atypical antipsychotics on neurocognition in euthymic bipolar patients. Compr Psychiatry 2011, 52(6):613-622.
  • [8]Arts B, Jabben N, Krabbendam L, Van Os J: A 2-year naturalistic study on cognitive functioning in bipolar disorder. Acta Psychiatr Scand 2011, 123(3):190-205.
  • [9]Keefe RS, Bilder RM, Davis SM, Harvey PD, Palmer BW, Gold JM, Meltzer HY, Green MF, Capuano G, Stroup TS, et al.: Neurocognitive effects of antipsychotic medications in patients with chronic schizophrenia in the CATIE Trial. Arch Gen Psychiatry 2007, 64(6):633-647.
  • [10]Keefe RS, Sweeney JA, Gu H, Hamer RM, Perkins DO, McEvoy JP, Lieberman JA: Effects of olanzapine, quetiapine, and risperidone on neurocognitive function in early psychosis: a randomized, double-blind 52-week comparison. Am J Psychiatry 2007, 164(7):1061-1071.
  • [11]Woodward ND, Purdon SE, Meltzer HY, Zald DH: A meta-analysis of cognitive change with haloperidol in clinical trials of atypical antipsychotics: dose effects and comparison to practice effects. Schizophr Res 2007, 89(1–3):211-224.
  • [12]Davidson M, Galderisi S, Weiser M, Werbeloff N, Fleischhacker WW, Keefe RS, Boter H, Keet IP, Prelipceanu D, Rybakowski JK, et al.: Cognitive effects of antipsychotic drugs in first-episode schizophrenia and schizophreniform disorder: a randomized, open-label clinical trial (EUFEST). Am J Psychiatry 2009, 166(6):675-682.
  • [13]Goldberg TE, Goldman RS, Burdick KE, Malhotra AK, Lencz T, Patel RC, Woerner MG, Schooler NR, Kane JM, Robinson DG: Cognitive improvement after treatment with second-generation antipsychotic medications in first-episode schizophrenia: is it a practice effect? Arch Gen Psychiatry 2007, 64(10):1115-1122.
  • [14]Guo X, Zhai J, Wei Q, Twamley EW, Jin H, Fang M, Hu M, Zhao J: Neurocognitive effects of first- and second-generation antipsychotic drugs in early-stage schizophrenia: a naturalistic 12-month follow-up study. Neurosci Lett 2011, 503(2):141-146.
  • [15]Howes OD, Kapur S: The dopamine hypothesis of schizophrenia: version III–the final common pathway. Schizophr Bull 2009, 35(3):549-562.
  • [16]Frank MJ, Fossella JA: Neurogenetics and pharmacology of learning, motivation, and cognition. Neuropsychopharmacology 2011, 36(1):133-152.
  • [17]Hariri AR: The what, where, and when of catechol-o-methyltransferase. Biol Psychiatry 2011, 70(3):214-215.
  • [18]Weickert TW, Goldberg TE, Mishara A, Apud JA, Kolachana BS, Egan MF, Weinberger DR: Catechol-O-methyltransferase val108/158met genotype predicts working memory response to antipsychotic medications. Biol Psychiatry 2004, 56(9):677-682.
  • [19]Bertolino A, Caforio G, Blasi G, De Candia M, Latorre V, Petruzzella V, Altamura M, Nappi G, Papa S, Callicott JH, et al.: Interaction of COMT (Val(108/158)Met) genotype and olanzapine treatment on prefrontal cortical function in patients with schizophrenia. Am J Psychiatry 2004, 161(10):1798-1805.
  • [20]Woodward ND, Jayathilake K, Meltzer HY: COMT val108/158met genotype, cognitive function, and cognitive improvement with clozapine in schizophrenia. Schizophr Res 2007, 90(1–3):86-96.
  • [21]Rebollo-Mesa I, Picchioni M, Shaikh M, Bramon E, Murray R, Toulopoulou T: COMT (Val(158/108)Met) genotype moderates the impact of antipsychotic medication on verbal IQ in twins with schizophrenia. Psychiatr Genet 2011, 21(2):98-105.
  • [22]Rosa EC, Dickinson D, Apud J, Weinberger DR, Elvevag B: COMT Val158Met polymorphism, cognitive stability and cognitive flexibility: an experimental examination. Behav Brain Funct 2010, 6:53. BioMed Central Full Text
  • [23]Jabben N, Arts B, Krabbendam L, Van Os J: Investigating the association between neurocognition and psychosis in bipolar disorder: further evidence for the overlap with schizophrenia. Bipolar Disord 2009, 11(2):166-177.
  • [24]APA: Diagnostic and Statistical Manual of Mental Disorders. Fourth edition. Washington, DC: American Psychiatric Association; 1994.
  • [25]McGuffin P, Farmer A, Harvey I: A polydiagnostic application of operational criteria in studies of psychotic illness. Development and reliability of the OPCRIT system. Arch Gen Psychiatry 1991, 48(8):764-770.
  • [26]Andreasen NC, Flaum M, Arndt S: The Comprehensive Assessment of Symptoms and History (CASH). An instrument for assessing diagnosis and psychopathology. Arch Gen Psychiatry 1992, 49(8):615-623.
  • [27]Maxwell ME: Manual for the family interview for genetic studies (FIGS). Bethesda, Maryland: National Institute of Mental Health; 1992.
  • [28]Goodwin GM, Anderson I, Arango C, Bowden CL, Henry C, Mitchell PB, Nolen WA, Vieta E, Wittchen HU: ECNP consensus meeting. Bipolar depression. Nice, March 2007. Eur Neuropsychopharmacol 2008, 18(7):535-549.
  • [29]Dickerson FB, Boronow JJ, Stallings C, Origoni AE, Cole S, Leister F, Krivogorsky B, Yolken RH: The catechol O-methyltransferase Val158Met polymorphism and herpes simplex virus type 1 infection are risk factors for cognitive impairment in bipolar disorder: additive gene-environmental effects in a complex human psychiatric disorder. Bipolar Disord 2006, 8(2):124-132.
  • [30]Diaz-Asper CM, Goldberg TE, Kolachana BS, Straub RE, Egan MF, Weinberger DR: Genetic variation in catechol-O-methyltransferase: effects on working memory in schizophrenic patients, their siblings, and healthy controls. Biol Psychiatry 2008, 63(1):72-79.
  • [31]Wirgenes KV, Djurovic S, Sundet K, Agartz I, Mattingsdal M, Athanasiu L, Melle I, Andreassen OA: Catechol O-methyltransferase variants and cognitive performance in schizophrenia and bipolar disorder versus controls. Schizophr Res 2010, 122(1–3):31-37.
  • [32]Luteijn F, van der Ploeg FAE: Handleiding Groninger Intelligentietest (GIT). Lisse, The Netherlands; 1983.
  • [33]Wechsler D: Wechsler Adult Intelligence Scale-Revised. New York: Psychological Corporation; 1981.
  • [34]Brand N, Jolles J: Learning and retrieval rate of words presented auditorily and visually. J Gen Psychol 1985, 112(2):201-210.
  • [35]Van der Elst W, Van Boxtel MP, Van Breukelen GJ, Jolles J: Rey’s verbal learning test: normative data for 1855 healthy participants aged 24–81 years and the influence of age, sex, education, and mode of presentation. J Int Neuropsychol Soc 2005, 11(3):290-302.
  • [36]Eriksen CW, Schultz DW: Information processing in visual search: a continuous flow conception and experimental results. Percept Psychophys 1979, 25(4):249-263.
  • [37]Wechsler D: WAIS-III: Wechsler Adult Intelligence Scale. In. San Antonio: Psychological Corporation; 1997.
  • [38]Van Winkel R: Family-based analysis of genetic variation underlying psychosis-inducing effects of cannabis: sibling analysis and proband follow-up. Arch Gen Psychiatry 2011, 68(2):148-157.
  • [39]StataCorp: STATA Statistical Software. In Release 8.0 edn. Texas: College Station; 2002.
  • [40]Snijders TAB, Bosker RJ: Multilevel Analysis, Second edition edn. London: SAGE Publications; 2002.
  • [41]Barnett JH, Scoriels L, Munafo MR: Meta-analysis of the cognitive effects of the catechol-O-methyltransferase gene Val158/108Met polymorphism. Biol Psychiatry 2008, 64(2):137-144.
  • [42]Tunbridge EM, Harrison PJ, Weinberger DR: Catechol-o-methyltransferase, cognition, and psychosis: Val158Met and beyond. Biol Psychiatry 2006, 60(2):141-151.
  • [43]Mata I, Perez-Iglesias R, Pelayo-Teran JM, Rodriguez-Sanchez JM, Gonzalez-Blanch C, Carrasco-Marin E, Vazquez-Barquero JL, Crespo-Facorro B: Lack of influence of COMT Val158Met genotype on cognition in first-episode non-affective psychosis. Schizophr Res 2008, 102(1–3):206-209.
  • [44]Barnett JH, Jones PB, Robbins TW, Muller U: Effects of the catechol-O-methyltransferase Val158Met polymorphism on executive function: a meta-analysis of the Wisconsin Card Sort Test in schizophrenia and healthy controls. Mol Psychiatry 2007, 12(5):502-509.
  • [45]Blanchard MM, Chamberlain SR, Roiser J, Robbins TW, Muller U: Effects of two dopamine-modulating genes (DAT1 9/10 and COMT Val/Met) on n-back working memory performance in healthy volunteers. Psychol Med 2011, 41(3):611-618.
  • [46]Krabbendam L, Isusi P, Galdos P, Echevarria E, Bilbao JR, Martin-Pagola A, Papiol S, Castano L, Van Os J: Associations between COMTVal158Met polymorphism and cognition: direct or indirect effects? Eur Psychiatry 2006, 21(5):338-342.
  • [47]Burdick KE, Funke B, Goldberg JF, Bates JA, Jaeger J, Kucherlapati R, Malhotra AK: COMT genotype increases risk for bipolar I disorder and influences neurocognitive performance. Bipolar Disord 2007, 9(4):370-376.
  • [48]Buckholtz JW, Sust S, Tan HY, Mattay VS, Straub RE, Meyer-Lindenberg A, Weinberger DR, Callicott JH: fMRI evidence for functional epistasis between COMT and RGS4. Mol Psychiatry 2007, 12(10):893-895. 885
  • [49]Prata DP, Mechelli A, Fu CH, Picchioni M, Toulopoulou T, Bramon E, Walshe M, Murray RM, Collier DA, McGuire P: Epistasis between the DAT 3’ UTR VNTR and the COMT Val158Met SNP on cortical function in healthy subjects and patients with schizophrenia. Proc Natl Acad Sci USA 2009, 106(32):13600-13605.
  • [50]Wishart HA, Roth RM, Saykin AJ, Rhodes CH, Tsongalis GJ, Pattin KA, Moore JH, McAllister TW: COMT Val158Met Genotype and Individual Differences in Executive Function in Healthy Adults. J Int Neuropsychol Soc 2011, 17(1):174-180.
  • [51]Straub RE, Lipska BK, Egan MF, Goldberg TE, Callicott JH, Mayhew MB, Vakkalanka RK, Kolachana BS, Kleinman JE, Weinberger DR: Allelic variation in GAD1 (GAD67) is associated with schizophrenia and influences cortical function and gene expression. Mol Psychiatry 2007, 12(9):854-869.
  • [52]Marenco S, Savostyanova AA, van der Veen JW, Geramita M, Stern A, Barnett AS, Kolachana B, Radulescu E, Zhang F, Callicott JH, et al.: Genetic modulation of GABA levels in the anterior cingulate cortex by GAD1 and COMT. Neuropsychopharmacology 2010, 35(8):1708-1717.
  • [53]Tan HY, Chen Q, Sust S, Buckholtz JW, Meyers JD, Egan MF, Mattay VS, Meyer-Lindenberg A, Weinberger DR, Callicott JH: Epistasis between catechol-O-methyltransferase and type II metabotropic glutamate receptor 3 genes on working memory brain function. Proc Natl Acad Sci USA 2007, 104(30):12536-12541.
  • [54]Nixon DC, Prust MJ, Sambataro F, Tan HY, Mattay VS, Weinberger DR, Callicott JH: Interactive effects of DAOA (G72) and catechol-O-methyltransferase on neurophysiology in prefrontal cortex. Biol Psychiatry 2011, 69(10):1006-1008.
  • [55]Opgen-Rhein C, Neuhaus AH, Urbanek C, Hahn E, Sander T, Dettling M: Executive attention in schizophrenic males and the impact of COMT Val108/158Met genotype on performance on the attention network test. Schizophr Bull 2008, 34(6):1231-1239.
  • [56]Bilder RM, Volavka J, Lachman HM, Grace AA: The catechol-O-methyltransferase polymorphism: relations to the tonic-phasic dopamine hypothesis and neuropsychiatric phenotypes. Neuropsychopharmacology 2004, 29(11):1943-1961.
  • [57]Durstewitz D, Seamans JK: The dual-state theory of prefrontal cortex dopamine function with relevance to catechol-o-methyltransferase genotypes and schizophrenia. Biol Psychiatry 2008, 64(9):739-749.
  • [58]Mier D, Kirsch P, Meyer-Lindenberg A: Neural substrates of pleiotropic action of genetic variation in COMT: a meta-analysis. Mol Psychiatry 2010, 15(9):918-927.
  • [59]Rasch B, Spalek K, Buholzer S, Luechinger R, Boesiger P, De Quervain DJ, Papassotiropoulos A: Aversive stimuli lead to differential amygdala activation and connectivity patterns depending on catechol-O-methyltransferase Val158Met genotype. Neuroimage 2010, 52(4):1712-1719.
  • [60]Williams LM, Gatt JM, Grieve SM, Dobson-Stone C, Paul RH, Gordon E, Schofield PR: COMT Val(108/158)Met polymorphism effects on emotional brain function and negativity bias. Neuroimage 2010, 53(3):918-925.
  • [61]Lelli-Chiesa G, Kempton MJ, Jogia J, Tatarelli R, Girardi P, Powell J, Collier DA, Frangou S: The impact of the Val158Met catechol- O-methyltransferase genotype on neural correlates of sad facial affect processing in patients with bipolar disorder and their relatives. Psychol Med 2011, 41(4):779-788.
  • [62]Dennis NA, Need AC, LaBar KS, Waters-Metenier S, Cirulli ET, Kragel J, Goldstein DB, Cabeza R: COMT val108/158 met genotype affects neural but not cognitive processing in healthy individuals. Cereb Cortex 2010, 20(3):672-683.
  • [63]Liu B, Song M, Li J, Liu Y, Li K, Yu C, Jiang T: Prefrontal-related functional connectivities within the default network are modulated by COMT val158met in healthy young adults. J Neurosci 2010, 30(1):64-69.
  • [64]Stokes PR, Rhodes RA, Grasby PM, Mehta MA: The Effects of The COMT val(108/158)met Polymorphism on BOLD Activation During Working Memory, Planning, and Response Inhibition: A Role for The Posterior Cingulate Cortex? Neuropsychopharmacology 2011, 36(4):763-771.
  • [65]Liu B, Li J, Yu C, Li Y, Liu Y, Song M, Fan M, Li K, Jiang T: Haplotypes of catechol-O-methyltransferase modulate intelligence-related brain white matter integrity. Neuroimage 2010, 50(1):243-249.
  • [66]Cools R, D’Esposito M: Inverted-U-shaped dopamine actions on human working memory and cognitive control. Biol Psychiatry 2011, 69(12):e113-e125.
  • [67]Cools R: Dopaminergic control of the striatum for high-level cognition. Curr Opin Neurobiol 2011, 21(3):402-407.
  • [68]Barnes SA, Young JW, Neill JC: D(1) receptor activation improves vigilance in rats as measured by the 5-choice continuous performance test. Psychopharmacology (Berl) 2011, 220(1):129-141.
  • [69]Van Holstein M, Aarts E, Van der Schaaf ME, Geurts DE, Verkes RJ, Franke B, Van Schouwenburg MR, Cools R: Human cognitive flexibility depends on dopamine D2 receptor signaling. Psychopharmacology (Berl) 2011, 218(3):567-578.
  • [70]Kurniawan IT, Guitart-Masip M, Dolan RJ: Dopamine and effort-based decision making. Front Neurosci 2011, 5:81.
  • [71]Aarts E, Van Holstein M, Cools R: Striatal Dopamine and the Interface between Motivation and Cognition. Front Psychol 2011, 2:163.
  • [72]Gamo NJ, Arnsten AF: Molecular modulation of prefrontal cortex: rational development of treatments for psychiatric disorders. Behav Neurosci 2011, 125(3):282-296.
  • [73]Ursini G, Bollati V, Fazio L, Porcelli A, Iacovelli L, Catalani A, Sinibaldi L, Gelao B, Romano R, Rampino A, et al.: Stress-related methylation of the catechol-O-methyltransferase Val 158 allele predicts human prefrontal cognition and activity. J Neurosci 2011, 31(18):6692-6698.
  • [74]Jacobs E, D’Esposito M: Estrogen shapes dopamine-dependent cognitive processes: implications for women’s health. J Neurosci 2011, 31(14):5286-5293.
  • [75]Karlsson S, Rieckmann A, Karlsson P, Farde L, Nyberg L, Backman L: Relationship of dopamine D1 receptor binding in striatal and extrastriatal regions to cognitive functioning in healthy humans. Neuroimage 2011, 57(2):346-351.
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