Skip to main content Accessibility help
×
Hostname: page-component-cd9895bd7-7cvxr Total loading time: 0 Render date: 2024-12-30T16:42:09.241Z Has data issue: false hasContentIssue false

Chapter 11 - Imaging Genetic and Epigenetic Markers in Mood Disorders

from Section 4 - Novel Approaches in Brain Imaging

Published online by Cambridge University Press:  12 January 2021

Sudhakar Selvaraj
Affiliation:
UTHealth School of Medicine, USA
Paolo Brambilla
Affiliation:
Università degli Studi di Milano
Jair C. Soares
Affiliation:
UT Harris County Psychiatric Center, USA
Get access

Summary

Genetics explain 60–85% and 31–50% of the risk to develop, respectively, bipolar disorder (BD) (1, 2) and major depressive disorder (MDD) (3, 4). Thus, hereditability has emerged as a crucial factor in the pathophysiology of mood disorders. Early genetics studies focused their attention on specific single-nucleotide polymorphism (SNP), preselected on prior evidence for their functional role in coding products that may influence relevant features of the disorders, also known as candidate gene approach. In these studies, we define risk allele, genetic variants associated with the disorder or worse clinical features such as reduced response to therapeutics, early onset, and higher recurrence.

Type
Chapter
Information
Mood Disorders
Brain Imaging and Therapeutic Implications
, pp. 135 - 150
Publisher: Cambridge University Press
Print publication year: 2021

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

Barnett, JH, Smoller, JW. The genetics of bipolar disorder. Neuroscience. 2009; 164(1): 331343.CrossRefGoogle ScholarPubMed
McGuffin, P, Rijsdijk, F, Andrew, M et al. The heritability of bipolar affective disorder and the genetic relationship to unipolar depression. Arch Gen Psychiatry. 2003; 60(5): 497502.CrossRefGoogle ScholarPubMed
Jansen, R, Penninx, BWJH, Madar, V, et al. Gene expression in major depressive disorder. Mol Psychiatr. 2016; 21(3): 339347.CrossRefGoogle ScholarPubMed
Hamet, P, Tremblay, J. Genetics and genomics of depression. Metabolism. 2005; 54 (5 Suppl 1): 1015.CrossRefGoogle ScholarPubMed
Chen, G, Henter, ID, Manji, HK. Translational research in bipolar disorder: Emerging insights from genetically based models. Mol Psychiatry. 2010; 15(9): 883895.CrossRefGoogle ScholarPubMed
Goes, FS. Genetics of bipolar disorder: Recent update and future directions. Psychiatr Clin North Am. 2016; 39(1): 139155.Google Scholar
Bogdan, R, Salmeron, BJ, Carey, CE, et al. Imaging genetics and genomics in psychiatry: A critical review of progress and potential. Biological Psychiatry. 2017; 82(3): 165175.CrossRefGoogle ScholarPubMed
Meyer-Lindenberg, A, Weinberger, DR. Intermediate phenotypes and genetic mechanisms of psychiatric disorders. Nat Rev Neurosci. 2006; 7(10): 818827.Google Scholar
Fusar-Poli, P, Howes, O, Bechdolf, A, Borgwardt, S. Mapping vulnerability to bipolar disorder: a systematic review and meta-analysis of neuroimaging studies. J Psychiatry Neurosci. 2012; 37(3): 170184.CrossRefGoogle ScholarPubMed
Piguet, C, Fodoulian, L, Aubry, JM, Vuilleumier, P, Houenou, J. Bipolar disorder: Functional neuroimaging markers in relatives. Neurosci Biobehav Rev. 2015; 57: 284296.CrossRefGoogle ScholarPubMed
Dima, D, Roberts, RE, Frangou, S. Connectomic markers of disease expression, genetic risk and resilience in bipolar disorder. Transl Psychiatry. 2016; 6: e706.CrossRefGoogle ScholarPubMed
Amico, F, Meisenzahl, E, Koutsouleris, N, et al. Structural MRI correlates for vulnerability and resilience to major depressive disorder. J Psychiatry Neurosci. 2011; 36(1): 1522.CrossRefGoogle ScholarPubMed
Huang, H, Fan, X, Williamson, DE, Rao, U. White matter changes in healthy adolescents at familial risk for unipolar depression: A diffusion tensor imaging study. Neuropsychopharmacology. 2011; 36(3): 684691.CrossRefGoogle ScholarPubMed
Kerner, B. Toward a deeper understanding of the genetics of bipolar disorder. Frontiers in Psychiatry. 2015; 6: 105.CrossRefGoogle Scholar
Sullivan, P, Wray, N, Consortium, PM. Genome-wide association analyses identify 44 risk variants and refine the genetic architecture of major depressive disorder. Eur Neuropsychopharm. 2019; 29: S805.CrossRefGoogle Scholar
Direk, N, Williams, S, Smith, JA, et al. An analysis of two genome-wide association meta-analyses identifies a new locus for broad depression phenotype. Biol Psychiat. 2017; 82(5): 322329.CrossRefGoogle ScholarPubMed
Hyde, CL, Nagle, MW, Tian, C, et al. Identification of 15 genetic loci associated with risk of major depression in individuals of European descent. Nature Genetics. 2016 September; 48(9): 10311036.CrossRefGoogle ScholarPubMed
Ikeda, M, Saito, T, Kondo, K, Iwata, N. Genome-wide association studies of bipolar disorder: A systematic review of recent findings and their clinical implications. Psychiatry Clin Neurosci. 2018; 72(2): 5263.CrossRefGoogle ScholarPubMed
Leal-Ortiz, S, Waites, CL, Terry-Lorenzo, R, et al. Piccolo modulation of Synapsin1a dynamics regulates synaptic vesicle exocytosis. Journal of Cell Biology. 2008; 181(5): 831846.CrossRefGoogle ScholarPubMed
Schuhmacher, A, Mossner, R, Hofels, S, et al. PCLO rs2522833 modulates HPA system response to antidepressant treatment in major depressive disorder. Int J Neuropsychoph. 2011; 14(2): 237245.CrossRefGoogle ScholarPubMed
Igata, R, Katsuki, A, Kakeda, S, et al. PCLO rs2522833-mediated gray matter volume reduction in patients with drug-naive, first-episode major depressive disorder. Transl Psychiatry. 2017 May 30; 7(5): e1140.CrossRefGoogle ScholarPubMed
Ryan, J, Artero, S, Carriere, I, et al. GWAS-identified risk variants for major depressive disorder: Preliminary support for an association with late-life depressive symptoms and brain structural alterations. Eur Neuropsychopharm. 2016; 26(1): 113125.CrossRefGoogle ScholarPubMed
Woudstra, S, Bochdanovits, Z, van Tol, MJ, et al. Piccolo genotype modulates neural correlates of emotion processing but not executive functioning. Transl Psychiatry. 2012; 2: e99.CrossRefGoogle Scholar
Woudstra, S, van Tol, MJ, Bochdanovits, Z, et al. Modulatory effects of the piccolo genotype on emotional memory in health and depression. PLoS One. 2013; 8(4): e61494.Google Scholar
Schott, BH, Assmann, A, Schmierer, P, et al. Epistatic interaction of genetic depression risk variants in the human subgenual cingulate cortex during memory encoding. Transl Psychiatry. 2014; 4: e372.CrossRefGoogle ScholarPubMed
Lewis, CM, Ng, MY, Butler, AW, et al. Genome-wide association study of major recurrent depression in the UK population. Am J Psychiat. 2010; 167(8): 949957.CrossRefGoogle Scholar
Bermingham, R, Carballedo, A, Lisiecka, D, et al. Effect of genetic variant in BICC1 on functional and structural brain changes in depression. Neuropsychopharmacology. 2012; 37(13): 28552862.CrossRefGoogle ScholarPubMed
Dannlowski, U, Kugel, H, Grotegerd, D, et al. NCAN cross-disorder risk variant is associated with limbic gray matter deficits in healthy subjects and major depression. Neuropsychopharmacology. 2015; 40(11): 25102516.CrossRefGoogle ScholarPubMed
Kim, BJ, Zaveri, HP, Shchelochkov, OA, et al. An allelic series of mice reveals a role for RERE in the development of multiple organs affected in chromosome 1p36 deletions. Plos One. 2013; 8(2): e57460.Google ScholarPubMed
Kakeda, S, Watanabe, K, Katsuki, A, et al. Genetic effects on white matter integrity in drug-naive patients with major depressive disorder: A diffusion tensor imaging study of 17 genetic loci associated with depressive symptoms. Neuropsych Dis Treat. 2019; 15: 375383.CrossRefGoogle ScholarPubMed
Han, KM, Won, E, Kang, J, et al. TESC gene-regulating genetic variant (rs7294919) affects hippocampal subfield volumes and parahippocampal cingulum white matter integrity in major depressive disorder. J Psychiat Res. 2017; 93: 2029.CrossRefGoogle ScholarPubMed
Cui, LL, Gong, XH, Tang, YQ, et al. Relationship between the LHPP gene polymorphism and resting-state brain activity in major depressive disorder. Neural Plasticity. 2016: 9162590.CrossRefGoogle Scholar
Ota, M, Hori, H, Sato, N, et al. Effects of ankyrin 3 gene risk variants on brain structures in patients with bipolar disorder and healthy subjects. Psychiatry Clin Neurosci. 2016; 70(11): 498506.CrossRefGoogle ScholarPubMed
Lippard, ETC, Jensen, KP, Wang, F, et al. Genetic variation of ANK3 is associated with lower white matter structural integrity in bipolar disorder. Mol Psychiatry. 2017; 22(9): 1225.CrossRefGoogle ScholarPubMed
Delvecchio, G, Dima, D, Frangou, S. The effect of ANK3 bipolar-risk polymorphisms on the working memory circuitry differs between loci and according to risk-status for bipolar disorder. Am J Med Genet B Neuropsychiatr Genet. 2015; 168B(3): 188196.CrossRefGoogle ScholarPubMed
Tesli, M, Egeland, R, Sonderby, IE, et al. No evidence for association between bipolar disorder risk gene variants and brain structural phenotypes. J Affect Disord. 2013; 151(1): 291297.CrossRefGoogle ScholarPubMed
Falls, DL. Neuregulins: Functions, forms, and signaling strategies. Exp Cell Res. 2003; 284(1): 1430.CrossRefGoogle ScholarPubMed
Cannon, DM, Walshe, M, Dempster, E, et al. The association of white matter volume in psychotic disorders with genotypic variation in NRG1, MOG and CNP: A voxel-based analysis in affected individuals and their unaffected relatives. Transl Psychiatry. 2012; 2: e167.CrossRefGoogle ScholarPubMed
Mechelli, A, Prata, DP, Fu, CH, et al. The effects of neuregulin1 on brain function in controls and patients with schizophrenia and bipolar disorder. Neuroimage. 2008; 42(2): 817826.CrossRefGoogle ScholarPubMed
Gomez-Ospina, N, Tsuruta, F, Barreto-Chang, O, Hu, L, Dolmetsch, R. The C terminus of the L-type voltage-gated calcium channel Ca(V)1.2 encodes a transcription factor. Cell. 2006; 127(3): 591606.CrossRefGoogle Scholar
Green, EK, Grozeva, D, Jones, I, et al. The bipolar disorder risk allele at CACNA1C also confers risk of recurrent major depression and of schizophrenia. Mol Psychiatr. 2010; 15(10): 10161022.CrossRefGoogle ScholarPubMed
Krug, A, Nieratschker, V, Markov, V, et al. Effect of CACNA1C rs1006737 on neural correlates of verbal fluency in healthy individuals. Neuroimage. 2010; 49(2): 18311836.CrossRefGoogle ScholarPubMed
Thimm, M, Kircher, T, Kellermann, T, et al. Effects of a CACNA1C genotype on attention networks in healthy individuals. Psychological Medicine. 2011; 41(7): 15511561.CrossRefGoogle ScholarPubMed
Backes, H, Dietsche, B, Nagels, A, et al. Genetic variation in CACNA1C affects neural processing in major depression. J Psychiat Res. 2014; 53: 3846.CrossRefGoogle ScholarPubMed
Soeiro-de-Souza, MG, Lafer, B, Moreno, RA, et al. The CACNA1C risk allele rs1006737 is associated with age-related prefrontal cortical thinning in bipolar I disorder. Transl Psychiatry. 2017; 7(4): e1086.Google Scholar
Perrier, E, Pompei, F, Ruberto, G, et al. Initial evidence for the role of CACNA1 C on subcortical brain morphology in patients with bipolar disorder. Eur Psychiatry. 2011; 26(3): 135137.CrossRefGoogle Scholar
Tesli, M, Skatun, KC, Ousdal, OT, et al. CACNA1C risk variant and amygdala activity in bipolar disorder, schizophrenia and healthy controls. PLoS One. 2013; 8(2): e56970.CrossRefGoogle ScholarPubMed
Dima, D, Jogia, J, Collier, D, et al. Independent modulation of engagement and connectivity of the facial network during affect processing by CACNA1C and ANK3 risk genes for bipolar disorder. JAMA Psychiatry. 2013; 70(12): 13031311.CrossRefGoogle ScholarPubMed
Jogia, J, Ruberto, G, Lelli-Chiesa, G, et al. The impact of the CACNA1C gene polymorphism on frontolimbic function in bipolar disorder. Mol Psychiatry. 2011; 16(11): 10701071.CrossRefGoogle ScholarPubMed
Whalley, HC, McKirdy, J, Romaniuk, L, et al. Functional imaging of emotional memory in bipolar disorder and schizophrenia. Bipolar Disord. 2009; 11(8): 840856.CrossRefGoogle ScholarPubMed
Bigos, KL, Mattay, VS, Callicott, JH, et al. Genetic variation in CACNA1C affects brain circuitries related to mental illness. Arch Gen Psychiatry. 2010; 67(9): 939945.CrossRefGoogle ScholarPubMed
Tecelao, D, Mendes, A, Martins, D, et al. The effect of psychosis associated CACNA1C, and its epistasis with ZNF804A, on brain function. Genes Brain Behav. 2019; 18(4): e12510.CrossRefGoogle ScholarPubMed
Mallas, E, Carletti, F, Chaddock, CA, et al. The impact of CACNA1C gene, and its epistasis with ZNF804A, on white matter microstructure in health, schizophrenia and bipolar disorder(1). Genes Brain Behav. 2017; 16(4): 479488.CrossRefGoogle ScholarPubMed
Soeiro-de-Souza, MG, Otaduy, MC, Dias, CZ, et al.The impact of the CACNA1C risk allele on limbic structures and facial emotions recognition in bipolar disorder subjects and healthy controls. J Affect Disord. 2012; 141(1): 94101.Google Scholar
Wolf, C, Mohr, H, Schneider-Axmann, T, et al. CACNA1 C genotype explains interindividual differences in amygdala volume among patients with schizophrenia. Eur Arch Psychiatry Clin Neurosci. 2014; 264(2): 93102.CrossRefGoogle Scholar
Radua, J, Surguladze, SA, Marshall, N, et al. The impact of CACNA1C allelic variation on effective connectivity during emotional processing in bipolar disorder. Mol Psychiatry. 2013; 18(5): 526527.Google Scholar
Byrne, EM, Carrillo-Roa, T, Penninx, BW, et al. Applying polygenic risk scores to postpartum depression. Arch Womens Ment Health. 2014; 17(6): 519528.Google Scholar
Levine, ME, Crimmins, EM, Prescott, CA, et al. A polygenic risk score associated with measures of depressive symptoms among older adults. Biodemogr Soc Biol. 2014; 60(2): 199211.CrossRefGoogle ScholarPubMed
Mullins, N, Power, RA, Fisher, HL, et al. Polygenic interactions with environmental adversity in the aetiology of major depressive disorder. Psychological Medicine. 2016; 46(4): 759770.CrossRefGoogle ScholarPubMed
Holmes, AJ, Lee, PH, Hollinshead, MO, et al. Individual differences in amygdala-medial prefrontal anatomy link negative affect, impaired social functioning, and polygenic depression risk. Journal of Neuroscience. 2012; 32(50): 1808718100.CrossRefGoogle ScholarPubMed
Whalley, HC, Sprooten, E, Hackett, S, et al. Polygenic risk and white matter integrity in individuals at high risk of mood disorder. Biol Psychiat. 2013; 74(4): 280286.CrossRefGoogle ScholarPubMed
Yuksel, D, Dietsche, B, Forstner, AJ, et al. Polygenic risk for depression and the neural correlates of working memory in healthy subjects. Prog Neuro-Psychoph. 2017; 79: 6776.CrossRefGoogle ScholarPubMed
Reus, LM, Shen, X, Gibson, J, et al. Association of polygenic risk for major psychiatric illness with subcortical volumes and white matter integrity in UK Biobank. Sci Rep-Uk. 2017; 7: 42140.CrossRefGoogle ScholarPubMed
Wigmore, EM, Clarke, TK, Howard, DM, et al. Do regional brain volumes and major depressive disorder share genetic architecture? A study of Generation Scotland (n=19762), UK Biobank (n=24048) and the English Longitudinal Study of Ageing (n=5766). Transl Psychiatry. 2017 August 15; 7(8): e1205.CrossRefGoogle Scholar
Wang, T, Zhang, X, Li, A, et al. Polygenic risk for five psychiatric disorders and cross-disorder and disorder-specific neural connectivity in two independent populations. NeuroImage Clinical. 2017; 14: 441449.CrossRefGoogle ScholarPubMed
Tesli, M, Kauppi, K, Bettella, F, et al. Altered brain activation during emotional face processing in relation to both diagnosis and polygenic risk of bipolar disorder. PLoS One. 2015; 10(7): e0134202.CrossRefGoogle ScholarPubMed
Dima, D, Breen, G. Polygenic risk scores in imaging genetics: Usefulness and applications. J Psychopharmacol. 2015; 29(8): 867871.CrossRefGoogle ScholarPubMed
Whalley, HC, Papmeyer, M, Sprooten, E, et al. The influence of polygenic risk for bipolar disorder on neural activation assessed using fMRI. Transl Psychiatry. 2012; 2: e130.CrossRefGoogle ScholarPubMed
Caseras, X, Tansey, KE, Foley, S, Linden, D. Association between genetic risk scoring for schizophrenia and bipolar disorder with regional subcortical volumes. Transl Psychiatry. 2015; 5: e692.Google Scholar
Wang, T, Zhang, X, Li, A, et al. Polygenic risk for five psychiatric disorders and cross-disorder and disorder-specific neural connectivity in two independent populations. Neuroimage Clin. 2017; 14: 441449.CrossRefGoogle ScholarPubMed
Doan, NT, Kaufmann, T, Bettella, F, et al. Distinct multivariate brain morphological patterns and their added predictive value with cognitive and polygenic risk scores in mental disorders. Neuroimage Clin. 2017; 15: 719731.CrossRefGoogle ScholarPubMed
Whalley, HC, Sprooten, E, Hackett, S, et al. Polygenic risk and white matter integrity in individuals at high risk of mood disorder. Biol Psychiatry. 2013; 74(4): 280286.CrossRefGoogle ScholarPubMed
Reus, LM, Shen, X, Gibson, J, et al. Association of polygenic risk for major psychiatric illness with subcortical volumes and white matter integrity in UK Biobank. Sci Rep. 2017; 7: 42140.Google Scholar
Sprooten, E, Fleming, KM, Thomson, PA, et al. White matter integrity as an intermediate phenotype: Exploratory genome-wide association analysis in individuals at high risk of bipolar disorder. Psychiatry Res. 2013; 206(2–3): 223231.CrossRefGoogle ScholarPubMed
Serretti, A, Cusin, C, Benedetti, F, et al. Insomnia improvement during antidepressant treatment and CLOCK gene polymorphism. Am J Med Genet B Neuropsychiatr Genet. 2005; 137B(1): 3639.CrossRefGoogle ScholarPubMed
Zai, CC, de Luca, V, Strauss, J, et al. Genetic factors and suicidal behavior. In: Dwivedi, Y, editor. The Neurobiological Basis of Suicide. Frontiers in Neuroscience. Boca Raton (FL) Florida, US: CRC Press/Taylor & Francis; 2012, p. 213.Google Scholar
Kenna, GA, Roder-Hanna, N, Leggio, L, et al. Association of the 5-HTT gene-linked promoter region (5-HTTLPR) polymorphism with psychiatric disorders: review of psychopathology and pharmacotherapy. Pharmgenomics Pers Med. 2012; 5: 1935.Google ScholarPubMed
Smeraldi, E, Benedetti, F, Zanardi, R. Serotonin transporter promoter genotype and illness recurrence in mood disorders. Eur Neuropsychopharmacol. 2002; 12(1): 7375.CrossRefGoogle ScholarPubMed
Serretti, A, Kato, M, De Ronchi, D, Kinoshita, T. Meta-analysis of serotonin transporter gene promoter polymorphism (5-HTTLPR) association with selective serotonin reuptake inhibitor efficacy in depressed patients. Mol Psychiatry. 2007; 12(3): 247257.CrossRefGoogle ScholarPubMed
Parra-Uribe, I, Blasco-Fontecilla, H, Garcia-Pares, G, et al. Risk of re-attempts and suicide death after a suicide attempt: A survival analysis. BMC Psychiatry. 2017; 17(1): 163.Google Scholar
Russ, MJ, Lachman, HM, Kashdan, T, Saito, T, Bajmakovic-Kacila, S. Analysis of catechol-O-methyltransferase and 5-hydroxytryptamine transporter polymorphisms in patients at risk for suicide. Psychiatry Res. 2000; 93(1): 7378.CrossRefGoogle ScholarPubMed
Murphy, SE, Norbury, R, Godlewska, BR, et al. The effect of the serotonin transporter polymorphism (5-HTTLPR) on amygdala function: A meta-analysis. Mol Psychiatry. 2013; 18(4): 512520.CrossRefGoogle ScholarPubMed
Munafo, MR, Brown, SM, Hariri, AR. Serotonin transporter (5-HTTLPR) genotype and amygdala activation: A meta-analysis. Biol Psychiatry. 2008; 63(9): 852857.CrossRefGoogle ScholarPubMed
Pezawas, L, Meyer-Lindenberg, A, Drabant, EM, et al. 5-HTTLPR polymorphism impacts human cingulate-amygdala interactions: A genetic susceptibility mechanism for depression. Nat Neurosci. 2005; 8(6): 828834.Google Scholar
Jonassen, R, Landro, NI. Serotonin transporter polymorphisms (5-HTTLPR) in emotion processing: Implications from current neurobiology. Prog Neurobiol. 2014; 117: 4153.CrossRefGoogle ScholarPubMed
Frodl, T, Zill, P, Baghai, T, et al. Reduced hippocampal volumes associated with the long variant of the tri- and diallelic serotonin transporter polymorphism in major depression. American Journal of Medical Genetics Part B, Neuropsychiatric Genetics: The Official Publication of the International Society of Psychiatric Genetics. 2008; 147B(7): 10031007.Google Scholar
Frodl, T, Meisenzahl, EM, Zill, P, et al. Reduced hippocampal volumes associated with the long variant of the serotonin transporter polymorphism in major depression. Arch Gen Psychiat. 2004; 61(2): 177183.CrossRefGoogle Scholar
Taylor, WD, Steffens, DC, Payne, ME, et al. Influence of serotonin transporter promoter region polymorphisms on hippocampal volumes in late-life depression. Arch Gen Psychiat. 2005; 62(5): 537544.CrossRefGoogle ScholarPubMed
Eker, MC, Kitis, O, Okur, H, et al. Smaller hippocampus volume is associated with short variant of 5-HTTLPR polymorphism in medication-free major depressive disorder patients. Neuropsychobiology. 2011; 63(1): 2228.CrossRefGoogle ScholarPubMed
Hickie, IB, Naismith, SL, Ward, PB, et al. Serotonin transporter gene status predicts caudate nucleus but not amygdala or hippocampal volumes in older persons with major depression. J Affect Disord. 2007; 98(1–2): 137142.CrossRefGoogle ScholarPubMed
Jaworska, N, MacMaster, FP, Foster, J, Ramasubbu, R. The influence of 5-HTTLPR and Val66 Met polymorphisms on cortical thickness and volume in limbic and paralimbic regions in depression: A preliminary study. BMC Psychiatry. 2016; 16: 61.CrossRefGoogle Scholar
Ahdidan, J, Foldager, L, Rosenberg, R, et al. Hippocampal volume and serotonin transporter polymorphism in major depressive disorder. Acta Neuropsychiatr. 2013; 25(4): 206214.CrossRefGoogle ScholarPubMed
Cole, J, Weinberger, DR, Mattay, VS, et al. No effect of 5HTTLPR or BDNF Val66 Met polymorphism on hippocampal morphology in major depression. Genes, Brain, and Behavior. 2011; 10(7): 756764.CrossRefGoogle ScholarPubMed
Hickie, IB, Naismith, SL, Ward, PB, et al. Serotonin transporter gene status predicts caudate nucleus but not amygdala or hippocampal volumes in older persons with major depression. J Affect Disorders. 2007; 98(1–2): 137142.CrossRefGoogle ScholarPubMed
Taylor, WD, Macfall, JR, Payne, ME, et al. Orbitofrontal cortex volume in late life depression: Influence of hyperintense lesions and genetic polymorphisms. Psychological Medicine. 2007; 37(12): 17631773.CrossRefGoogle ScholarPubMed
Costafreda, SG, McCann, P, Saker, P, et al. Modulation of amygdala response and connectivity in depression by serotonin transporter polymorphism and diagnosis. J Affect Disorders. 2013; 150(1): 96103.CrossRefGoogle ScholarPubMed
Dannlowski, U, Ohrmann, P, Bauer, J, et al. 5-HTTLPR biases amygdala activity in response to masked facial expressions in major depression. Neuropsychopharmacology: Official Publication of the American College of Neuropsychopharmacology. 2008; 33(2): 418424.CrossRefGoogle ScholarPubMed
Friedel, E, Schlagenhauf, F, Sterzer, P, et al. 5-HTT genotype effect on prefrontal-amygdala coupling differs between major depression and controls. Psychopharmacology. 2009; 205(2): 261271.CrossRefGoogle ScholarPubMed
Benedetti, F, Bollettini, I, Poletti, S, et al. White matter microstructure in bipolar disorder is influenced by the serotonin transporter gene polymorphism 5-HTTLPR. Genes Brain Behav. 2015; 14(3): 238250.Google Scholar
Frodl, T, Reinhold, E, Koutsouleris, N, et al. Childhood stress, serotonin transporter gene and brain structures in major depression. Neuropsychopharmacology: Official publication of the American College of Neuropsychopharmacology. 2010; 35(6): 13831390.CrossRefGoogle ScholarPubMed
Alexopoulos, GS, Murphy, CF, Gunning-Dixon, FM, et al. Serotonin transporter polymorphisms, microstructural white matter abnormalities and remission of geriatric depression. J Affect Disorders. 2009; 119(1–3): 132141.CrossRefGoogle ScholarPubMed
Parsey, RV, Olvet, DM, Oquendo, MA, et al. Higher 5-HT1A receptor binding potential during a major depressive episode predicts poor treatment response: Preliminary data from a naturalistic study. Neuropsychopharmacology. 2006; 31(8): 17451749.CrossRefGoogle Scholar
Lemonde, S, Turecki, G, Bakish, D, et al. Impaired repression at a 5-hydroxytryptamine 1 A receptor gene polymorphism associated with major depression and suicide. The Journal of Neuroscience. 2003; 23(25): 87888799.Google Scholar
Vai, B, Riberto, M, Ghiglino, D, et al. A 5-HT1Areceptor promoter polymorphism influences fronto-limbic functional connectivity and depression severity in bipolar disorder. Psychiatry Res Neuroimaging. 2017; 270: 17.CrossRefGoogle Scholar
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): 19431961.CrossRefGoogle Scholar
Benedetti, F, Dallaspezia, S, Colombo, C, et al. Effect of catechol-O-methyltransferase Val(108/158)Met polymorphism on antidepressant efficacy of fluvoxamine. Eur Psychiatry. 2010; 25(8): 476478.CrossRefGoogle ScholarPubMed
Benedetti, F, Barbini, B, Bernasconi, A, et al. Acute antidepressant response to sleep deprivation combined with light therapy is influenced by the catechol-O-methyltransferase Val(108/158)Met polymorphism. J Affect Disord. 2010; 121(1–2): 6872.CrossRefGoogle ScholarPubMed
Benedetti, F, Dallaspezia, S, Locatelli, C, et al. Recurrence of bipolar mania is associated with catechol-O-methyltransferase Val(108/158)Met polymorphism. J Affect Disord. 2011; 132(1–2): 293296.CrossRefGoogle ScholarPubMed
Benedetti, F, Dallaspezia, S, Colombo, C, et al. Association between catechol-O-methyltransferase Val(108/158)Met polymorphism and psychotic features of bipolar disorder. J Affect Disord. 2010; 125(1–3): 341344.CrossRefGoogle ScholarPubMed
Papolos, DF, Veit, S, Faedda, GL, Saito, T, Lachman, HM. Ultra-ultra rapid cycling bipolar disorder is associated with the low activity catecholamine-O-methyltransferase allele. Mol Psychiatry. 1998; 3(4): 346349.Google Scholar
Seok, JH, Choi, S, Lim, HK, et al. Effect of the COMT val158 met polymorphism on white matter connectivity in patients with major depressive disorder. Neurosci Lett. 2013; 545: 3539.CrossRefGoogle Scholar
Hayashi, K, Yoshimura, R, Kakeda, S, et al. COMT Val158 Met, but not BDNF Val66 Met, is associated with white matter abnormalities of the temporal lobe in patients with first-episode, treatment-naive major depressive disorder: A diffusion tensor imaging study. Neuropsych Dis Treat. 2014; 10: 11831190.Google Scholar
Watanabe, K, Kakeda, S, Yoshimura, R, et al. Relationship between the catechol-O-methyl transferase Va1108/158 Met genotype and brain volume in treatment-naive major depressive disorder: Voxel-based morphometry analysis. Psychiat Res-Neuroim. 2015; 233(3): 481487.CrossRefGoogle Scholar
Opmeer, EM, Kortekaas, R, van Tol, MJ, et al. Influence of COMT val158 met genotype on the depressed brain during emotional processing and working memory. PLoS One. 2013; 8(9): e73290.CrossRefGoogle Scholar
Vai, B, Riberto, M, Poletti, S, et al. Catechol-O-methyltransferase Val (108/158) Met polymorphism affects fronto-limbic connectivity during emotional processing in bipolar disorder. European Psychiatry. 2017; 41: 5359.Google Scholar
Miskowiak, KW, Kjaerstad, HL, Stottrup, MM, et al. The catechol-O-methyltransferase (COMT) Val158 Met genotype modulates working memory-related dorsolateral prefrontal response and performance in bipolar disorder. Bipolar Disord. 2017; 19(3): 214224.CrossRefGoogle Scholar
Hempstead, BL. Brain-derived neurotrophic factor: Three ligands, many actions. Trans Am Clin Climatol Assoc. 2015; 126: 919.Google ScholarPubMed
Notaras, M, Hill, R, van den Buuse, M. The BDNF gene Val66 Met polymorphism as a modifier of psychiatric disorder susceptibility: Progress and controversy. Mol Psychiatry. 2015; 20(8): 916930.CrossRefGoogle Scholar
Ide, S, Kakeda, S, Watanabe, K, et al. Relationship between a BDNF gene polymorphism and the brain volume in treatment-naive patients with major depressive disorder: A VBM analysis of brain MRI. Psychiatry Res. 2015; 233(2): 120124.CrossRefGoogle ScholarPubMed
Legge, RM, Sendi, S, Cole, JH, et al. Modulatory effects of brain-derived neurotrophic factor Val66 Met polymorphism on prefrontal regions in major depressive disorder. Br J Psychiatry. 2015; 206(5): 379384.CrossRefGoogle Scholar
Frodl, T, Schule, C, Schmitt, G, et al. Association of the brain-derived neurotrophic factor Val66 Met polymorphism with reduced hippocampal volumes in major depression. Arch Gen Psychiatry. 2007; 64(4): 410416.CrossRefGoogle Scholar
Carballedo, A, Morris, D, Zill, P, et al. Brain-derived neurotrophic factor Val66 Met polymorphism and early life adversity affect hippocampal volume. Am J Med Genet B Neuropsychiatr Genet. 2013; 162B(2): 183190.CrossRefGoogle Scholar
Youssef, MM, Underwood, MD, Huang, YY, et al. Association of BDNF Val66 Met polymorphism and brain BDNF levels with major depression and suicide. Int J Neuropsychopharmacol. 2018; 21(6): 528538.CrossRefGoogle Scholar
Alexopoulos, GS, Glatt, CE, Hoptman, MJ, et al. BDNF val66 met polymorphism, white matter abnormalities and remission of geriatric depression. J Affect Disord. 2010; 125(1–3): 262268.Google Scholar
Han, KM, Choi, S, Kim, A, et al. The effects of 5-HTTLPR and BDNF Val66 Met polymorphisms on neurostructural changes in major depressive disorder. Psychiatry Res Neuroimaging. 2018; 273: 2534.CrossRefGoogle Scholar
Tatham, EL, Hall, GBC, Clark, D, Foster, J, Ramasubbu, R. The 5-HTTLPR and BDNF polymorphisms moderate the association between uncinate fasciculus connectivity and antidepressants treatment response in major depression. European Archives of Psychiatry and Clinical Neuroscience. 2017; 267(2): 135147.CrossRefGoogle ScholarPubMed
Yin, YY, Hou, ZH, Wang, XQ, Sui, YX, Yuan, YG. The BDNF Val66 Met polymorphism, resting-state hippocampal functional connectivity and cognitive deficits in acute late-onset depression. J Affect Disorders. 2015; 183: 2230.CrossRefGoogle Scholar
Opmeer, EM, Kortekaas, R, van Tol, MJ, et al. Influence of COMT val158 met genotype on the depressed brain during emotional processing and working memory. Plos One. 2013 September 12; 8(9): e73290.CrossRefGoogle Scholar
Gonul, AS, Kitis, O, Eker, MC, et al. Association of the brain-derived neurotrophic factor Val66 Met polymorphism with hippocampus volumes in drug-free depressed patients. World J Biol Psychia. 2011; 12(2): 110118.CrossRefGoogle Scholar
Kanellopoulos, D, Gunning, FM, Morimoto, SS, et al. Hippocampal volumes and the brain-derived neurotrophic factor val66 met polymorphism in geriatric major depression. Am J Geriatr Psychiatry. 2011; 19(1): 1322.Google Scholar
Cao, B, Bauer, IE, Sharma, AN, et al. Reduced hippocampus volume and memory performance in bipolar disorder patients carrying the BDNF val66 met met allele. J Affect Disord. 2016; 198: 198205.CrossRefGoogle Scholar
Chepenik, LG, Fredericks, C, Papademetris, X, et al. Effects of the brain-derived neurotrophic growth factor val66 met variation on hippocampus morphology in bipolar disorder. Neuropsychopharmacology. 2009; 34(4): 944951.CrossRefGoogle Scholar
Matsuo, K, Walss-Bass, C, Nery, FG, et al. Neuronal correlates of brain-derived neurotrophic factor Val66 Met polymorphism and morphometric abnormalities in bipolar disorder. Neuropsychopharmacology. 2009; 34(8): 19041913.CrossRefGoogle Scholar
Mirakhur, A, Moorhead, TW, Stanfield, AC, et al. Changes in gyrification over 4 years in bipolar disorder and their association with the brain-derived neurotrophic factor valine(66) methionine variant. Biol Psychiatry. 2009; 66(3): 293297.CrossRefGoogle ScholarPubMed
Zeni, CP, Mwangi, B, Cao, B, et al. Interaction between BDNF rs6265 Met allele and low family cohesion is associated with smaller left hippocampal volume in pediatric bipolar disorder. J Affect Disord. 2016; 189: 9497.CrossRefGoogle ScholarPubMed
Mandolini, GM, Lazzaretti, M, Pigoni, A, et al. The impact of BDNF Val66 Met polymorphism on cognition in bipolar disorder: A review: Special section on “translational and neuroscience studies in affective disorders” section editor, Maria Nobile MD, PhD. This section of JAD focuses on the relevance of translational and neuroscience studies in providing a better understanding of the neural basis of affective disorders. The main aim is to briefly summaries relevant research findings in clinical neuroscience with particular regards to specific innovative topics in mood and anxiety disorders. J Affect Disord. 2019; 243: 552558.CrossRefGoogle Scholar
Fernandes, BS, Molendijk, ML, Kohler, CA, et al. Peripheral brain-derived neurotrophic factor (BDNF) as a biomarker in bipolar disorder: a meta-analysis of 52 studies. BMC Med. 2015; 13: 289.CrossRefGoogle ScholarPubMed
Chen, J, Xu, Y, Zhang, J, et al. Genotypic association of the DAOA gene with resting-state brain activity in major depression. Mol Neurobiol. 2012; 46(2): 361373.CrossRefGoogle ScholarPubMed
Choi, S, Han, KM, Kang, J, et al. Effects of a polymorphism of the neuronal amino acid transporter SLC6A15 gene on structural integrity of white matter tracts in major depressive disorder. Plos One. 2016 October 10; 11(10): e0164301.CrossRefGoogle ScholarPubMed
Wang, LJ, Liu, ZF, Cao, XH, et al. A combined study of SLC6A15 gene polymorphism and the resting-state functional magnetic resonance imaging in first-episode drug-naive major depressive disorder. Genet Test Mol Bioma. 2017; 21(9): 523530.Google Scholar
Poletti, S, Riberto, M, Vai, B, et al. A glutamate transporter EAAT1 gene variant influences amygdala functional connectivity in bipolar disorder. Journal of Molecular Neuroscience. 2018; 65(4): 536545.Google Scholar
Poletti, S, Bollettini, I, Lorenzi, C, et al. White matter microstructure in bipolar disorder is influenced by the interaction between a glutamate transporter EAAT1 gene variant and early stress. Molecular Neurobiology. 2018: 19.CrossRefGoogle Scholar
Benedetti, F, Poletti, S, Locatelli, C, et al. A Homer 1 gene variant influences brain structure and function, lithium effects on white matter, and antidepressant response in bipolar disorder: A multimodal genetic imaging study. Progress in Neuro-Psychopharmacology and Biological Psychiatry. 2018; 81: 8895.CrossRefGoogle Scholar
Benedetti, F, Poletti, S, Locatelli, C, et al. A Homer 1 gene variant influences brain structure and function, lithium effects on white matter, and antidepressant response in bipolar disorder: A multimodal genetic imaging study. Prog Neuropsychopharmacol Biol Psychiatry. 2018; 81: 8895.CrossRefGoogle Scholar
Bollettini, I, Melloni, EMT, Aggio, V, et al. Clock genes associate with white matter integrity in depressed bipolar patients. Chronobiology International. 2017; 34(2): 212224.CrossRefGoogle ScholarPubMed
Poletti, S, Aggio, V, Bollettini, I, et al. SREBF-2 polymorphism influences white matter microstructure in bipolar disorder. Psychiatry Research: Neuroimaging. 2016; 257: 3946.CrossRefGoogle ScholarPubMed
Grimes, CA, Jope, RS. CREB DNA binding activity is inhibited by glycogen synthase kinase-3 beta and facilitated by lithium. J Neurochem. 2001; 78(6): 12191232.Google Scholar
Inkster, B, Nichols, TE, Saemann, PG, et al. Association of GSK3beta polymorphisms with brain structural changes in major depressive disorder. Arch Gen Psychiatry. 2009; 66(7): 721728.CrossRefGoogle ScholarPubMed
Inkster, B, Simmons, A, Cole, JH, et al. Unravelling the GSK3 beta-related genotypic interaction network influencing hippocampal volume in recurrent major depressive disorder. Psychiatric Genetics. 2018; 28(5): 7784.CrossRefGoogle Scholar
Liu, Z, Guo, H, Cao, XH, et al. A combined study of GSK3 beta polymorphisms and brain network topological metrics in major depressive disorder. Psychiat Res-Neuroim. 2014; 223(3): 210217.CrossRefGoogle ScholarPubMed
Inkster, B, Nichols, TE, Saemann, PG, et al. Pathway-based approaches to imaging genetics association studies: Wnt signaling, GSK3beta substrates and major depression. Neuroimage. 2010; 53(3): 908917.CrossRefGoogle ScholarPubMed
Benedetti, F, Serretti, A, Colombo, C, et al. A glycogen synthase kinase 3-beta promoter gene single nucleotide polymorphism is associated with age at onset and response to total sleep deprivation in bipolar depression. Neurosci Lett. 2004; 368(2): 123126.CrossRefGoogle ScholarPubMed
Benedetti, F, Bollettini, I, Barberi, I, et al. Lithium and GSK3-β promoter gene variants influence white matter microstructure in bipolar disorder. Neuropsychopharmacology. 2013; 38(2): 313.CrossRefGoogle ScholarPubMed
Horstmann, S, Lucae, S, Menke, A, et al. Polymorphisms in GRIK4, HTR2A, and FKBP5 show interactive effects in predicting remission to antidepressant treatment. Neuropsychopharmacology. 2010; 35(3): 727740.CrossRefGoogle ScholarPubMed
Binder, EB, Salyakina, D, Lichtner, P, et al. Polymorphisms in FKBP5 are associated with increased recurrence of depressive episodes and rapid response to antidepressant treatment. Nat Genet. 2004; 36(12): 13191325.CrossRefGoogle ScholarPubMed
Pace, TW, Miller, AH. Cytokines and glucocorticoid receptor signaling. Relevance to major depression. Ann N Y Acad Sci. 2009; 1179: 86105.CrossRefGoogle ScholarPubMed
Cordova-Palomera, A, de Reus, MA, Fatjo-Vilas, M, et al. FKBP5 modulates the hippocampal connectivity deficits in depression: A study in twins. Brain Imaging Behav. 2017; 11(1): 6275.CrossRefGoogle ScholarPubMed
Tozzi, L, Carballedo, A, Wetterling, F, et al. Single-nucleotide polymorphism of the FKBP5 gene and childhood maltreatment as predictors of structural changes in brain areas involved in emotional processing in depression. Neuropsychopharmacology. 2016; 41(2): 487497.CrossRefGoogle ScholarPubMed
Han, KM, Won, E, Sim, Y, et al. Influence of FKBP5 polymorphism and DNA methylation on structural changes of the brain in major depressive disorder. Sci Rep-Uk. 2017; 7.Google Scholar
Tozzi, L, Doolin, K, Farrel, C, et al. Functional magnetic resonance imaging correlates of emotion recognition and voluntary attentional regulation in depression: A generalized psycho-physiological interaction study. J Affect Disorders. 2017; 208: 535544.Google Scholar
Qiu, AQ, Taylor, WD, Zhao, Z, et al. APOE related hippocampal shape alteration in geriatric depression. Neuroimage. 2009; 44(3): 620626.CrossRefGoogle ScholarPubMed
Kim, DH, Payne, ME, Levy, RM, MacFall, JR, Steffens, DC. APOE genotype and hippocampal volume change in geriatric depression. Biol Psychiat. 2002; 51(5): 426429.CrossRefGoogle ScholarPubMed
Sachs-Ericsson, N, Sawyer, K, Corsentino, E, Collins, N, Steffens, DC. The moderating effect of the APOE epsilon 4 allele on the relationship between hippocampal volume and cognitive decline in older depressed patients. Am J Geriat Psychiat. 2011; 19(1): 2332.CrossRefGoogle Scholar
Yuan, YG, Zhang, ZJ, Bai, F, et al. Genetic variation in apolipoprotein E alters regional gray matter volumes in remitted late-onset depression. J Affect Disorders. 2010; 121(3): 273277.Google Scholar
Shu, H, Yuan, YG, Xie, CM, et al. Imbalanced hippocampal functional networks associated with remitted geriatric depression and apolipoprotein E epsilon 4 allele in nondemented elderly: A preliminary study. J Affect Disorders. 2014; 164: 513.CrossRefGoogle Scholar
Wu, D, Yuan, YG, Ba, F, et al. Abnormal functional connectivity of the default mode network in remitted late-onset depression. J Affect Disorders. 2013; 147(1–3): 277287.CrossRefGoogle ScholarPubMed
Chang, KJ, Hong, CH, Lee, KS, et al. Differential effects of white matter hyperintensity on geriatric depressive symptoms according to APOE-epsilon 4 status. J Affect Disorders. 2015; 188: 2834.CrossRefGoogle Scholar
Lavretsky, H, Lesser, IM, Wohl, M, et al. Apolipoprotein-E and white matter hyperintensities in late-life depression. Am J Geriat Psychiat. 2000; 8(3): 257261.CrossRefGoogle ScholarPubMed
Turecki, G, Ota, VK, Belangero, SI, Jackowski, A, Kaufman, J. Early life adversity, genomic plasticity, and psychopathology. Lancet Psychiatry. 2014; 1(6): 461466.CrossRefGoogle ScholarPubMed
Lutz, PE, Turecki, G. DNA methylation and childhood maltreatment: From animal models to human studies. Neuroscience. 2014; 264: 142156.CrossRefGoogle ScholarPubMed
Szyf, M. The early life social environment and DNA methylation: DNA methylation mediating the long-term impact of social environments early in life. Epigenetics. 2011; 6(8): 971978.CrossRefGoogle ScholarPubMed
Caspi, A, Hariri, AR, Holmes, A, Uher, R, Moffitt, TE. Genetic sensitivity to the environment: The case of the serotonin transporter gene and its implications for studying complex diseases and traits. Am J Psychiatry. 2010; 167(5): 509527.CrossRefGoogle Scholar
Philibert, RA, Sandhu, H, Hollenbeck, N, et al. The relationship of 5HTT (SLC6A4) methylation and genotype on mRNA expression and liability to major depression and alcohol dependence in subjects from the Iowa adoption studies. Am J Med Genet B Neuropsychiatr Genet. 2008; 147B(5): 543549.CrossRefGoogle ScholarPubMed
Okada, S, Morinobu, S, Fuchikami, M, et al. The potential of SLC6A4 gene methylation analysis for the diagnosis and treatment of major depression. J Psychiatr Res. 2014; 53: 4753.CrossRefGoogle ScholarPubMed
Domschke, K, Tidow, N, Schwarte, K, et al. Serotonin transporter gene hypomethylation predicts impaired antidepressant treatment response. Int J Neuropsychopharmacol. 2014; 17(8): 11671176.CrossRefGoogle ScholarPubMed
Olsson, CA, Foley, DL, Parkinson-Bates, M, et al. Prospects for epigenetic research within cohort studies of psychological disorder: A pilot investigation of a peripheral cell marker of epigenetic risk for depression. Biol Psychol. 2010; 83(2): 159165.CrossRefGoogle ScholarPubMed
Kang, HJ, Kim, JM, Stewart, R, et al. Association of SLC6A4 methylation with early adversity, characteristics and outcomes in depression. Prog Neuropsychopharmacol Biol Psychiatry. 2013; 44: 2328.CrossRefGoogle ScholarPubMed
Sugawara, H, Iwamoto, K, Bundo, M, et al. Hypermethylation of serotonin transporter gene in bipolar disorder detected by epigenome analysis of discordant monozygotic twins. Transl Psychiatry. 2011; 1: e24.CrossRefGoogle ScholarPubMed
Won, E, Choi, S, Kang, J, et al. Association between reduced white matter integrity in the corpus callosum and serotonin transporter gene DNA methylation in medication-naive patients with major depressive disorder. Transl Psychiatry. 2016; 6(8): e866.Google Scholar
Booij, L, Szyf, M, Carballedo, A, et al. DNA methylation of the serotonin transporter gene in peripheral cells and stress-related changes in hippocampal volume: A study in depressed patients and healthy controls. PLoS One. 2015; 10(3): e0119061.CrossRefGoogle ScholarPubMed
Kaer, K, Speek, M. Retroelements in human disease. Gene. 2013; 518(2): 231241.CrossRefGoogle ScholarPubMed
Schneider, I, Kugel, H, Redlich, R, et al. Association of serotonin transporter gene AluJb methylation with major depression, amygdala responsiveness, 5-HTTLPR/rs25531 polymorphism, and stress. Neuropsychopharmacology. 2018; 43(6): 13081316.CrossRefGoogle ScholarPubMed
Na, KS, Won, E, Kang, J, et al. Differential effect of COMT gene methylation on the prefrontal connectivity in subjects with depression versus healthy subjects. Neuropharmacology. 2018; 137: 5970.CrossRefGoogle ScholarPubMed
Tyrka, AR, Ridout, KK, Parade, SH. Childhood adversity and epigenetic regulation of glucocorticoid signaling genes: Associations in children and adults. Dev Psychopathol. 2016; 28(4pt2): 13191331.CrossRefGoogle ScholarPubMed
Tozzi, L, Farrell, C, Booij, L, et al. Epigenetic changes of FKBP5 as a link connecting genetic and environmental risk factors with structural and functional brain changes in major depression. Neuropsychopharmacology. 2018; 43(5): 11381145.Google Scholar
Han, KM, Won, E, Sim, Y, et al. Influence of FKBP5 polymorphism and DNA methylation on structural changes of the brain in major depressive disorder. Sci Rep. 2017; 7: 42621.CrossRefGoogle ScholarPubMed
Na, KS, Chang, HS, Won, E, et al. Association between glucocorticoid receptor methylation and hippocampal subfields in major depressive disorder. PLoS One. 2014; 9(1): e85425.CrossRefGoogle ScholarPubMed
Palma-Gudiel, H, Cordova-Palomera, A, Tornador, C, et al. Increased methylation at an unexplored glucocorticoid responsive element within exon 1D of NR3C1 gene is related to anxious-depressive disorders and decreased hippocampal connectivity. Eur Neuropsychopharmacol. 2018; 28(5): 579588.CrossRefGoogle ScholarPubMed
Fuchikami, M, Morinobu, S, Segawa, M, et al. DNA methylation profiles of the brain-derived neurotrophic factor (BDNF) gene as a potent diagnostic biomarker in major depression. PLoS One. 2011; 6(8): e23881.Google Scholar
Tadic, A, Muller-Engling, L, Schlicht, KF, et al. Methylation of the promoter of brain-derived neurotrophic factor exon IV and antidepressant response in major depression. Mol Psychiatry. 2014; 19(3): 281283.CrossRefGoogle ScholarPubMed
Kang, HJ, Kim, JM, Lee, JY, et al. BDNF promoter methylation and suicidal behavior in depressive patients. J Affect Disord. 2013; 151(2): 679685.CrossRefGoogle ScholarPubMed
Martinowich, K, Hattori, D, Wu, H, et al. DNA methylation-related chromatin remodeling in activity-dependent BDNF gene regulation. Science. 2003; 302(5646): 890893.CrossRefGoogle ScholarPubMed
Choi, S, Han, KM, Won, E, et al. Association of brain-derived neurotrophic factor DNA methylation and reduced white matter integrity in the anterior corona radiata in major depression. J Affect Disord. 2015; 172: 7480.CrossRefGoogle ScholarPubMed
Han, KM, Won, E, Kang, J, et al. TESC gene-regulating genetic variant (rs7294919) affects hippocampal subfield volumes and parahippocampal cingulum white matter integrity in major depressive disorder. J Psychiatr Res. 2017; 93: 2029.CrossRefGoogle ScholarPubMed

Save book to Kindle

To save this book to your Kindle, first ensure no-reply@cambridge.org is added to your Approved Personal Document E-mail List under your Personal Document Settings on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part of your Kindle email address below. Find out more about saving to your Kindle.

Note you can select to save to either the @free.kindle.com or @kindle.com variations. ‘@free.kindle.com’ emails are free but can only be saved to your device when it is connected to wi-fi. ‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.

Find out more about the Kindle Personal Document Service.

Available formats
×

Save book to Dropbox

To save content items to your account, please confirm that you agree to abide by our usage policies. If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account. Find out more about saving content to Dropbox.

Available formats
×

Save book to Google Drive

To save content items to your account, please confirm that you agree to abide by our usage policies. If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account. Find out more about saving content to Google Drive.

Available formats
×