Genetic neuroimaging of bipolar disorder: a systematic 2017-2020 update.


Journal

Psychiatric genetics
ISSN: 1473-5873
Titre abrégé: Psychiatr Genet
Pays: England
ID NLM: 9106748

Informations de publication

Date de publication:
01 04 2021
Historique:
pubmed: 26 1 2021
medline: 15 12 2021
entrez: 25 1 2021
Statut: ppublish

Résumé

There is evidence of genetic polymorphism influences on brain structure and function, genetic risk in bipolar disorder (BD), and neuroimaging correlates of BD. How genetic influences related to BD could be reflected on brain changes in BD has been efficiently reviewed in a 2017 systematic review. We aimed to confirm and extend these findings through a Preferred Reporting Items for Systematic reviews and Meta-Analyses-based systematic review. Our study allowed us to conclude that there is no replicated finding in the timeframe considered. We were also unable to further confirm prior results of the BDNF gene polymorphisms to affect brain structure and function in BD. The most consistent finding is an influence of the CACNA1C rs1006737 polymorphism in brain connectivity and grey matter structure and function. There was a tendency of undersized studies to obtain positive results and large, genome-wide polygenic risk studies to find negative results in BD. The neuroimaging genetics in BD field is rapidly expanding.

Identifiants

pubmed: 33492063
doi: 10.1097/YPG.0000000000000274
pii: 00041444-202104000-00002
doi:

Substances chimiques

CACNA1C protein, human 0
Calcium Channels, L-Type 0

Types de publication

Journal Article Meta-Analysis Systematic Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

50-64

Informations de copyright

Copyright © 2021 Wolters Kluwer Health, Inc. All rights reserved.

Références

Abé C, Liberg B, Song J, Bergen SE, Petrovic P, Ekman CJ, et al. (2020). Longitudinal cortical thickness changes in bipolar disorder and the relationship to genetic risk, mania, and lithium use. Biol Psychiatry. 87:271–281.
Arts B, Simons CJ, van Os J (2013). Evidence for the impact of the CACNA1C risk allele rs1006737 on 2-year cognitive functioning in bipolar disorder. Psychiatr Genet. 23:41–42.
Baj G, Carlino D, Gardossi L, Tongiorgi E (2013). Toward a unified biological hypothesis for the BDNF Val66Met-associated memory deficits in humans: a model of impaired dendritic mRNA trafficking. Front Neurosci. 7:188.
Bastos CR, Tovo-Rodrigues L, Ardais AP, Xavier J, Salerno PSV, Camerini L, et al. (2020). The role of CACNA1C gene and childhood trauma interaction on bipolar disorder. Prog Neuropsychopharmacol Biol Psychiatry. 101:109915.
Bath KG, Lee FS (2006). Variant BDNF (Val66Met) impact on brain structure and function. Cogn Affect Behav Neurosci. 6:79–85.
Benedetti F, Serretti A, Colombo C, Barbini B, Lorenzi C, Campori E, et al. (2003). Influence of CLOCK gene polymorphism on circadian mood fluctuation and illness recurrence in bipolar depression. Am J Med Genet B Neuropsychiatr Genet. 123B:23–26.
Benedetti F, Dallaspezia S, Colombo C, Lorenzi C, Pirovano A, Smeraldi E (2010). Association between catechol-O-methyltransferase Val(108/158)Met polymorphism and psychotic features of bipolar disorder. J Affect Disord. 125:341–344.
Benedetti F, Poletti S, Locatelli C, Mazza E, Lorenzi C, Vitali A, et al. (2018). 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. 81:88–95.
Benned-Jensen T, Christensen RK, Denti F, Perrier JF, Rasmussen HB, Olesen SP (2016). Live imaging of Kv7.2/7.3 cell surface dynamics at the axon initial segment: high steady-state stability and calpain-dependent excitotoxic downregulation revealed. J Neurosci. 36:2261–2266.
Bhat S, Dao DT, Terrillion CE, Arad M, Smith RJ, Soldatov NM, Gould TD (2012). CACNA1C (Cav1.2) in the pathophysiology of psychiatric disease. Prog Neurobiol. 99:1–14.
Bollettini I, Melloni EM, Aggio V, Poletti S, Lorenzi C, Pirovano A, et al. (2017). Clock genes associate with white matter integrity in depressed bipolar patients. Chronobiol Int. 34:212–224.
Buraei Z, Yang J (2013). Structure and function of the β subunit of voltage-gated Ca² + channels. Biochim Biophys Acta. 1828:1530–1540.
Calabrò M, Mandelli L, Crisafulli C, Lee SJ, Jun TY, Wang SM, et al. (2018). Neuroplasticity, neurotransmission and brain-related genes in major depression and bipolar disorder: focus on treatment outcomes in an Asiatic sample. Adv Ther. 35:1656–1670.
Calabrò M, Mandelli L, Crisafulli C, Nicola MD, Colombo R, Janiri L, et al. (2020). ZNF804A gene variants have a cross-diagnostic influence on psychosis and treatment improvement in mood disorders. Clin Psychopharmacol Neurosci. 18:231–240.
Cao B, Bauer IE, Sharma AN, Mwangi B, Frazier T, Lavagnino L, et al. (2016). Reduced hippocampus volume and memory performance in bipolar disorder patients carrying the BDNF val66met m et al lele. J Affect Disord. 198:198–205.
Cao B, Passos IC, Mwangi B, Amaral-Silva H, Tannous J, Wu MJ, et al. (2017). Hippocampal subfield volumes in mood disorders. Mol Psychiatry. 22:1352–1358.
Chang EH, Kirtley A, Chandon TS, Borger P, Husain-Krautter S, Vingtdeux V, Malhotra AK (2015). Postnatal neurodevelopmental expression and glutamate-dependent regulation of the ZNF804A rodent homologue. Schizophr Res. 168:402–410.
Chao MV (2003). Neurotrophins and their receptors: a convergence point for many signalling pathways. Nat Rev Neurosci. 4:299–309.
Chen G, Henter ID, Manji HK (2010). Presynaptic glutamatergic dysfunction in bipolar disorder. Biol Psychiatry. 67:1007–1009.
Chen J, Tan J, Greenshaw AJ, Sawalha J, Liu Y, Zhang X, et al. (2020). CACNB2 rs11013860 polymorphism correlates of prefrontal cortex thickness in bipolar patients with first-episode mania. J Affect Disord. 268:82–87.
Chepenik LG, Fredericks C, Papademetris X, Spencer L, Lacadie C, Wang F, et al. (2009). Effects of the brain-derived neurotrophic growth factor val66met variation on hippocampus morphology in bipolar disorder. Neuropsychopharmacology. 34:944–951.
Cherlyn SY, Woon PS, Liu JJ, Ong WY, Tsai GC, Sim K (2010). Genetic association studies of glutamate, GABA and related genes in schizophrenia and bipolar disorder: a decade of advance. Neurosci Biobehav Rev. 34:958–977.
Cirelli C, Gutierrez CM, Tononi G (2004). Extensive and divergent effects of sleep and wakefulness on brain gene expression. Neuron. 41:35–43.
Clinton SM, Meador-Woodruff JH (2004). Abnormalities of the NMDA receptor and associated intracellular molecules in the thalamus in schizophrenia and bipolar disorder. Neuropsychopharmacology. 29:1353–1362.
Codd V, Nelson CP, Albrecht E, Mangino M, Deelen J, Buxton JL, et al.; CARDIoGRAM consortium. (2013). Identification of seven loci affecting mean telomere length and their association with disease. Nat Genet. 45:422–7, 427e1.
Collins MO, Husi H, Yu L, Brandon JM, Anderson CN, Blackstock WP, et al. (2006). Molecular characterization and comparison of the components and multiprotein complexes in the postsynaptic proteome. J Neurochem. 97 (Suppl 1):16–23.
Corradini I, Verderio C, Sala M, Wilson MC, Matteoli M (2009). SNAP-25 in neuropsychiatric disorders. Ann N Y Acad Sci. 1152:93–99.
Craddock N, Sklar P (2013). Genetics of bipolar disorder. Lancet. 381:1654–1662.
Cross-Disorder Group of the Psychiatric Genomics Consortium (2013). Identification of risk loci with shared effects on five major psychiatric disorders: a genome-wide analysis. Lancet. 381:1371–1379. Erratum in: Lancet 381(9875):1360. Erratum in Lancet 381:1360.
Cuomo I, Kotzalidis GD, De Filippis S (2017). Clinical stabilisation with lacosamide of mood disorder comorbid with PTSD and fronto-temporal epilepsy. Acta Biomed. 88:185–189.
Cupertino RB, Kappel DB, Bandeira CE, Schuch JB, da Silva BS, Müller D, et al. (2016). SNARE complex in developmental psychiatry: neurotransmitter exocytosis and beyond. J Neural Transm (Vienna). 123:867–883.
Curtis D, Vine AE, McQuillin A, Bass NJ, Pereira A, Kandaswamy R, et al. (2011). Case-case genome-wide association analysis shows markers differentially associated with schizophrenia and bipolar disorder and implicates calcium channel genes. Psychiatr Genet. 21:1–4.
Dallaspezia S, Benedetti F (2009). Melatonin, circadian rhythms, and the clock genes in bipolar disorder. Curr Psychiatry Rep. 6:488–493.
Dallaspezia S, Locatelli C, Lorenzi C, Pirovano A, Colombo C, Benedetti F (2016). Sleep homeostatic pressure and PER3 VNTR gene polymorphism influence antidepressant response to sleep deprivation in bipolar depression. J Affect Disord. 192:64–69.
Delvecchio G, Dima D, Frangou S (2015). 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. 168B:188–196.
Dietsche B, Backes H, Laneri D, Weikert T, Witt SH, Rietschel M, et al. (2014). The impact of a CACNA1C gene polymorphism on learning and hippocampal formation in healthy individuals: a diffusion tensor imaging study. Neuroimage. 89:256–261.
Dijk DJ, Archer SN (2010). PERIOD3, circadian phenotypes, and sleep homeostasis. Sleep Med Rev. 3:151–160.
Dima D, Jogia J, Collier D, Vassos E, Burdick KE, Frangou S (2013). Independent modulation of engagement and connectivity of the facial network during affect processing by CACNA1C and ANK3 risk genes for bipolar disorder. JAMA Psychiatry. 70:1303–1311.
Doan NT, Kaufmann T, Bettella F, Jørgensen KN, Brandt CL, Moberget T, et al. (2017). Distinct multivariate brain morphological patterns and their added predictive value with cognitive and polygenic risk scores in mental disorders. Neuroimage Clin. 15:719–731.
Durak O, de Anda FC, Singh KK, Leussis MP, Petryshen TL, Sklar P, Tsai LH (2015). Ankyrin-G regulates neurogenesis and Wnt signaling by altering the subcellular localization of β-catenin. Mol Psychiatry. 20:388–397.
Ebisawa T, Uchiyama M, Kajimura N, Mishima K, Kamei Y, Katoh M, et al. (2001). Association of structural polymorphisms in the human period3 gene with delayed sleep phase syndrome. EMBO Rep. 4:342–346.
Egan MF, Goldberg TE, Kolachana BS, Callicott JH, Mazzanti CM, Straub RE, et al. (2001). Effect of COMT Val108/158 Met genotype on frontal lobe function and risk for schizophrenia. Proc Natl Acad Sci U S A. 98:6917–6922.
Ferreira MA, O’Donovan MC, Meng YA, Jones IR, Ruderfer DM, Jones L, et al.; Wellcome Trust Case Control Consortium (2008). Collaborative genome-wide association analysis supports a role for ANK3 and CACNA1C in bipolar disorder. Nat Genet. 40:1056–1058.
Green EK, Hamshere M, Forty L, Gordon-Smith K, Fraser C, Russell E, et al.; WTCCC (2013). Replication of bipolar disorder susceptibility alleles and identification of two novel genome-wide significant associations in a new bipolar disorder case-control sample. Mol Psychiatry. 18:1302–1307.
Guo X, Liu D, Wang T, Luo X (2019). Aetiology of bipolar disorder: contribution of the L-type voltage-gated calcium channels. Gen Psychiatr. 32:e100009.
Hatzimanolis A, Smyrnis N, Avramopoulos D, Stefanis CN, Evdokimidis I, Stefanis NC (2012). Bipolar disorder ANK3 risk variant effect on sustained attention is replicated in a large healthy population. Psychiatr Genet. 22:210–213.
Han MR, Han KM, Kim A, Kang W, Kang Y, Kang J, et al. (2019). Whole-exome sequencing identifies variants associated with structural MRI markers in patients with bipolar disorders. J Affect Disord. 249:159–168.
Heinrich A, Müller KU, Banaschewski T, Barker GJ, Bokde ALW, Bromberg U, et al.; IMAGEN consortium (2016). Prediction of alcohol drinking in adolescents: personality-traits, behavior, brain responses, and genetic variations in the context of reward sensitivity. Biol Psychol. 118:79–87.
Hibar DP, Westlye LT, van Erp TG, Rasmussen J, Leonardo CD, Faskowitz J, et al.; Costa Rica/Colombia Consortium for Genetic Investigation of Bipolar Endophenotypes (2016). Subcortical volumetric abnormalities in bipolar disorder. Mol Psychiatry. 21:1710–1716.
Hibar DP, Westlye LT, Doan NT, Jahanshad N, Cheung JW, Ching CRK, et al. (2018). Cortical abnormalities in bipolar disorder: an MRI analysis of 6503 individuals from the ENIGMA Bipolar Disorder Working Group. Mol Psychiatry. 23:932–942.
Higgins GA, Allyn-Feuer A, Barbour E, Athey BD (2015). A glutamatergic network mediates lithium response in bipolar disorder as defined by epigenome pathway analysis. Pharmacogenomics. 16:1547–1563.
Hill MJ, Jeffries AR, Dobson RJ, Price J, Bray NJ (2012). Knockdown of the psychosis susceptibility gene ZNF804A alters expression of genes involved in cell adhesion. Hum Mol Genet. 21:1018–1024.
Hopp SC (2020). Targeting microglia L-type voltage-dependent calcium channels for the treatment of central nervous system disorders. J Neurosci Res.
Hori H, Yamamoto N, Teraishi T, Ota M, Fujii T, Sasayama D, et al. (2014). Cognitive effects of the ANK3 risk variants in patients with bipolar disorder and healthy individuals. J Affect Disord. 158:90–96.
Hørlyck LD, Macoveanu J, Vinberg M, Kessing LV, Siebner HR, Miskowiak KW (2019). The BDNF Val66Met polymorphism has no effect on encoding-related hippocampal response but influences recall in remitted patients with bipolar disorder. Front Psychiatry. 10:845.
Hoseth EZ, Krull F, Dieset I, Mørch RH, Hope S, Gardsjord ES, et al. (2018). Exploring the Wnt signaling pathway in schizophrenia and bipolar disorder. Transl Psychiatry. 8:55.
Houenou J, Boisgontier J, Henrion A, d’Albis MA, Dumaine A, Linke J, et al. (2017). A multilevel functional study of a SNAP25 at-risk variant for bipolar disorder and schizophrenia. J Neurosci. 37:10389–10397.
Jan WC, Yang SY, Chuang LC, Lu RB, Lu MK, Sun HS, Kuo PH (2014). Exploring the associations between genetic variants in genes encoding for subunits of calcium channel and subtypes of bipolar disorder. J Affect Disord. 157:80–86.
Janiri D, Di Nicola M, Martinotti G, Janiri L (2017). Who’s the leader, mania or depression? Predominant polarity and alcohol/polysubstance use in bipolar disorders. Curr Neuropharmacol. 15:409–416.
Janiri D, Moser DA, Doucet GE, Luber MJ, Rasgon A, Lee WH, et al. (2019a). Shared neural phenotypes for mood and anxiety disorders: a meta-analysis of 226 task-related functional imaging studies. JAMA Psychiatry. 77:1–8.
Janiri D, Simonetti A, Piras F, Ciullo V, Spalletta G, Sani G. (2019b). Predominant polarity and hippocampal subfield volumes in bipolar disorders. Bipolar Disord.
Janiri D, Sani G, De Rossi P, Piras F, Banaj N, Ciullo V, et al. (2019c). Hippocampal subfield volumes and childhood trauma in bipolar disorders. J Affect Disord. 253:35–43.
Kabir ZD, Martínez-Rivera A, Rajadhyaksha AM (2017). From gene to behavior: L-type calcium channel mechanisms underlying neuropsychiatric symptoms. Neurotherapeutics. 14:588–613.
Karthikeyan R, Marimuthu G, Ramasubramanian C, Arunachal G, BaHammam AS, Spence DW, et al. (2014). Association of Per3 length polymorphism with bipolar I disorder and schizophrenia. Neuropsychiatr Dis Treat. 10:2325–2330.
Kato T (2007). Molecular genetics of bipolar disorder and depression. Psychiatry Clin Neurosci. 61:3–19.
Kempton MJ, Ruberto G, Vassos E, Tatarelli R, Girardi P, Collier D, Frangou S (2009). Effects of the CACNA1C risk allele for bipolar disorder on cerebral gray matter volume in healthy individuals. Am J Psychiatry. 166:1413–1414.
Kotzalidis GD, Rapinesi C, Savoja V, Cuomo I, Simonetti A, Ambrosi E, et al. (2017). Neurobiological evidence for the primacy of mania hypothesis. Curr Neuropharmacol. 15:339–352.
Lancaster TM, Foley S, Tansey KE, Linden DE, Caseras X (2016). CACNA1C risk variant is associated with increased amygdala volume. Eur Arch Psychiatry Clin Neurosci. 266:269–275.
Leal G, Bramham CR, Duarte CB (2017). BDNF and hippocampal synaptic plasticity. Vitam Horm. 104:153–195.
Leber SL, Llenos IC, Miller CL, Dulay JR, Haybaeck J, Weis S (2017). Homer1a protein expression in schizophrenia, bipolar disorder, and major depression. J Neural Transm (Vienna). 124:1261–1273.
Lee MT, Chen CH, Lee CS, Chen CC, Chong MY, Ouyang WC, et al. (2011). Genome-wide association study of bipolar I disorder in the Han Chinese population. Mol Psychiatry. 16:548–556.
Leitch B, Szostek A, Lin R, Shevtsova O (2009). Subcellular distribution of L-type calcium channel subtypes in rat hippocampal neurons. Neuroscience. 164:641–657.
Leussis MP, Madison JM, Petryshen TL (2012). Ankyrin 3: genetic association with bipolar disorder and relevance to disease pathophysiology. Biol Mood Anxiety Disord. 2:18.
Leussis MP, Berry-Scott EM, Saito M, Jhuang H, de Haan G, Alkan O, et al. (2013). The ANK3 bipolar disorder gene regulates psychiatric-related behaviors that are modulated by lithium and stress. Biol Psychiatry. 73:683–690.
Lim CH, Zain SM, Reynolds GP, Zain MA, Roffeei SN, Zainal NZ, et al. (2014). Genetic association of LMAN2L gene in schizophrenia and bipolar disorder and its interaction with ANK3 gene polymorphism. Prog Neuropsychopharmacol Biol Psychiatry. 54:157–162.
Linke J, Witt SH, King AV, Nieratschker V, Poupon C, Gass A, et al. (2012). Genome-wide supported risk variant for bipolar disorder alters anatomical connectivity in the human brain. Neuroimage. 59:3288–3296.
Lippard ETC, Jensen KP, Wang F, Johnston JAY, Spencer L, Pittman B, et al. (2017). Effects of ANK3 variation on gray and white matter in bipolar disorder. Mol Psychiatry. 22:1345–1351.
Liu C, Zhang L, Wu J, Sui X, Xu Y, Huang L, et al. (2017). AnkG hemizygous mice present cognitive impairment and elevated anxiety/depressive-like traits associated with decreased expression of GABA receptors and postsynaptic density protein. Exp Brain Res. 235:3375–3390.
Liu F, Gong X, Yao X, Cui L, Yin Z, Li C, et al. (2019). Variation in the CACNB2 gene is associated with functional connectivity of the Hippocampus in bipolar disorder. BMC Psychiatry. 19:62.
Liu YS, Dai X, Wu W, Yuan FF, Gu X, Chen JG, et al. (2017). The association of SNAP25 gene polymorphisms in attention deficit/hyperactivity disorder: a systematic review and meta-analysis. Mol Neurobiol. 54:2189–2200.
Machado-Vieira R, Ibrahim L, Henter ID, Zarate CA Jr (2012). Novel glutamatergic agents for major depressive disorder and bipolar disorder. Pharmacol Biochem Behav. 100:678–687.
Mallas EJ, Carletti F, Chaddock CA, Woolley J, Picchioni MM, Shergill SS, et al. (2016). Genome-wide discovered psychosis-risk gene ZNF804A impacts on white matter microstructure in health, schizophrenia and bipolar disorder. PeerJ. 4:e1570.
Mallas E, Carletti F, Chaddock CA, Shergill S, Woolley J, Picchioni MM, et al. (2017). The impact of CACNA1C gene, and its epistasis with ZNF804A, on white matter microstructure in health, schizophrenia and bipolar disorder1. Genes Brain Behav. 16:479–488.
Mandolini GM, Lazzaretti M, Pigoni A, Delvecchio G, Soares JC, Brambilla P (2019). The impact of BDNF Val66Met 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. 243:552–558.
Mehrafza S, Kermanshahi S, Mostafidi S, Motaghinejad M, Motevalian M, Fatima S (2019). Pharmacological evidence for lithium-induced neuroprotection against methamphetamine-induced neurodegeneration via Akt-1/GSK3 and CREB-BDNF signaling pathways. Iran J Basic Med Sci. 22:856–865.
Miskowiak KW, Kjaerstad HL, Støttrup MM, Svendsen AM, Demant KM, Hoeffding LK, et al. (2017). The catechol-O-methyltransferase (COMT) Val158Met genotype modulates working memory-related dorsolateral prefrontal response and performance in bipolar disorder. Bipolar Disord. 19:214–224.
Moher D, Liberati A, Tetzlaff J, Altman DG; PRISMA Group (2009). Preferred reporting items for systematic reviews and meta-analyses: the PRISMA statement. Plos Med. 6:e1000097.
Muneer A (2017). Wnt and GSK3 signaling pathways in bipolar disorder: clinical and therapeutic implications. Clin Psychopharmacol Neurosci. 15:100–114.
Mynett-Johnson LA, Murphy VE, Claffey E, Shields DC, McKeon P (1998). Preliminary evidence of an association between bipolar disorder in females and the catechol-O-methyltransferase gene. Psychiatr Genet. 8:221–225.
Najera K, Fagan BM, Thompson PM (2019). SNAP-25 in major psychiatric disorders: a review. Neuroscience. 420:79–85.
Nanavati D, Austin DR, Catapano LA, Luckenbaugh DA, Dosemeci A, Manji HK, et al. (2011). The effects of chronic treatment with mood stabilizers on the rat hippocampal post-synaptic density proteome. J Neurochem. 119:617–629.
Nanou E, Catterall WA (2018). Calcium channels, synaptic plasticity, and neuropsychiatric disease. Neuron. 98:466–481.
Numakawa T, Odaka H, Adachi N (2018). Actions of brain-derived neurotrophin factor in the neurogenesis and neuronal function, and its involvement in the pathophysiology of brain diseases. Int J Mol Sci. 19:3650.
Ota M, Hori H, Sato N, Yoshida F, Hattori K, Teraishi T, Kunugi H (2016). Effects of ankyrin 3 gene risk variants on brain structures in patients with bipolar disorder and healthy subjects. Psychiatry Clin Neurosci. 70:498–506.
Parkin GM, Udawela M, Gibbons A, Dean B (2018). Glutamate transporters, EAAT1 and EAAT2, are potentially important in the pathophysiology and treatment of schizophrenia and affective disorders. World J Psychiatry. 8:51–63.
Pereira LP, Köhler CA, de Sousa RT, Solmi M, de Freitas BP, Fornaro M, et al. (2017). The relationship between genetic risk variants with brain structure and function in bipolar disorder: a systematic review of genetic-neuroimaging studies. Neurosci Biobehav Rev. 79:87–109.
Poletti S, Riberto M, Vai B, Ghiglino D, Lorenzi C, Vitali A, et al. (2018). A glutamate transporter EAAT1 gene variant influences amygdala functional connectivity in bipolar disorder. J Mol Neurosci. 65:536–545.
Poletti S, Bollettini I, Lorenzi C, Vitali A, Brioschi S, Serretti A, et al. (2019). White matter microstructure in bipolar disorder is influenced by the interaction between a glutamate transporter EAAT1 gene variant and early stress. Mol Neurobiol. 56:702–710.
Powell TR, Dima D, Frangou S, Breen G (2018). Telomere length and bipolar disorder. Neuropsychopharmacology. 43:445–453. Erratum in Neuropsychopharmacology 43:454.
Powell TR, De Jong S, Breen G, Lewis CM, Dima D (2019). Telomere length as a predictor of emotional processing in the brain. Hum Brain Mapp. 40:1750–1759.
Psychiatric GWAS Consortium Bipolar Disorder Working Group (2011). Large-scale genome-wide association analysis of bipolar disorder identifies a new susceptibility locus near ODZ4. Nat Genet. 43:977–983. Erratum in: Nat Genet. 2012 Sep;44(9):1072.
Qiao J, Rong L, Wang Z, Zhang M (2017). Involvement of Akt/GSK3β/CREB signaling pathway on chronic omethoate induced depressive-like behavior and improvement effects of combined lithium chloride and astaxanthin treatment. Neurosci Lett. 649:55–61.
Ranlund S, Rosa MJ, de Jong S, Cole JH, Kyriakopoulos M, Fu CHY, et al. (2018). Associations between polygenic risk scores for four psychiatric illnesses and brain structure using multivariate pattern recognition. Neuroimage Clin. 20:1026–1036.
Rao S, Siu CO, Shi M, Zhang J, Lam MHB, Yu M, et al. (2018). Associations of homer scaffolding protein 1 gene and psychological correlates with suicide attempts in Chinese: a pilot study of multifactorial risk model. Gene. 679:382–388.
Redecker TM, Kisko TM, Wöhr M, Schwarting RKW (2020). CACNA1C haploinsufficiency lacks effects on adult hippocampal neurogenesis and volumetric properties of prefrontal cortex and hippocampus in female rats. Physiol Behav. 223:112974.
Rietschel M, Mattheisen M, Frank J, Treutlein J, Degenhardt F, Breuer R, et al. (2010). Genome-wide association-, replication-, and neuroimaging study implicates HOMER1 in the etiology of major depression. Biol Psychiatry. 68:578–585.
Roby Y (2017). ANK3 gene polymorphisms and bipolar disorder: a meta-analysis. Psychiatr Genet. 27:225–235.
Rodríguez-Ramírez AM, Meza-Urzúa F, Cedillo-Ríos V, Becerra-Palar C, Jiménez-Pavón J, Morales-Cedillo IP, et al. (2020). CACNA1C risk variant and mood stabilizers effects in the prefrontal cortical thickness of Mexican patients with bipolar disorder. Neuropsychiatr Dis Treat. 16:1199–1206.
Roussos P, Katsel P, Davis KL, Bitsios P, Giakoumaki SG, Jogia J, et al. (2012). Molecular and genetic evidence for abnormalities in the nodes of Ranvier in schizophrenia. Arch Gen Psychiatry. 69:7–15.
Roussos P, Mitchell AC, Voloudakis G, Fullard JF, Pothula VM, Tsang J, et al. (2014). A role for noncoding variation in schizophrenia. Cell Rep. 9:1417–1429.
Ruberto G, Vassos E, Lewis CM, Tatarelli R, Girardi P, Collier D, Frangou S (2011). The cognitive impact of the ANK3 risk variant for bipolar disorder: initial evidence of selectivity to signal detection during sustained attention. PLoS One. 6:e16671.
Rybakowski JK, Borkowska A, Skibinska M, Szczepankiewicz A, Kapelski P, Leszczynska-Rodziewicz A, et al. (2006). Prefrontal cognition in schizophrenia and bipolar illness in relation to Val66Met polymorphism of the brain-derived neurotrophic factor gene. Psychiatry Clin Neurosci. 60:70–76.
Sani G, Napoletano F, Forte AM, Kotzalidis GD, Panaccione I, Porfiri GM, et al. (2012). The wnt pathway in mood disorders. Curr Neuropharmacol. 10:239–253.
Sani G, Simonetti A, Janiri D, Banaj N, Ambrosi E, De Rossi P, et al. (2018). Association between duration of lithium exposure and hippocampus/amygdala volumes in type I bipolar disorder. J Affect Disord. 232:341–348.
Schizophrenia Psychiatric Genome-Wide Association Study (GWAS) Consortium (2011). Genome-wide association study identifies five new schizophrenia loci. Nat Genet. 43:969–976.
Schizophrenia Working Group of the Psychiatric Genomics Consortium; Ripke S, Neale BM, Corvin A, Walter JTR, Farh K-H, Holmans PA, et al. (2014). Biological insights from 108 schizophrenia-associated genetic loci. Nature. 511:421–427.
Schultz CC, Nenadic I, Riley B, Vladimirov VI, Wagner G, Koch K, et al. (2014). ZNF804A and cortical structure in schizophrenia: in vivo and postmortem studies. Schizophr Bull. 40:532–541.
Schulze TG, Detera-Wadleigh SD, Akula N, Gupta A, Kassem L, Steele J, et al.; NIMH Genetics Initiative Bipolar Disorder Consortium. (2009). Two variants in Ankyrin 3 ( ANK3 ) are independent genetic risk factors for bipolar disorder. Mol Psychiatry. 14:487–491.
Serretti A, Cusin C, Benedetti F, Mandelli L, Pirovano A, Zanardi R, et al. (2005) Insomnia improvement during antidepressant treatment and CLOCK gene polymorphism. Am J Med Genet B Neuropsychiatr Genet. 137B:36–39.
Shi J, Wittke-Thompson JK, Badner JA, Hattori E, Potash JB, Willour VL, et al. (2008) Clock genes may influence bipolar disorder susceptibility and dysfunctional circadian rhythm. Am J Med Genet B Neuropsychiatr Genet. 147:1047–1055.
Shonibare DO, Patel R, Islam AH, Metcalfe AWS, Fiksenbaum L, Kennedy JL, et al. (2020). Preliminary study of structural magnetic resonance imaging phenotypes related to genetic variation in Interleukin-1β rs16944 in adolescents with Bipolar Disorder. J Psychiatr Res. 122:33–41.
Simões B, Vassos E, Shergill S, McDonald C, Toulopoulou T, Kalidindi S, et al. (2020). Schizophrenia polygenic risk score influence on white matter microstructure. J Psychiatr Res. 121:62–67.
Smedler E, Abé C, Pålsson E, Ingvar M, Landén M (2019). CACNA1C polymorphism and brain cortical structure in bipolar disorder. J Psychiatry Neurosci. 45:182–187.
Smith KR, Kopeikina KJ, Fawcett-Patel JM, Leaderbrand K, Gao R, Schürmann B, et al. (2014). Psychiatric risk factor ANK3 /ankyrin-G nanodomains regulate the structure and function of glutamatergic synapses. Neuron. 84:399–415.
Soeiro-de-Souza MG, Lafer B, Moreno RA, Nery FG, Chile T, Chaim K, da Costa Leite C, et al. (2017). The CACNA1C risk allele rs1006737 is associated with age-related prefrontal cortical thinning in bipolar I disorder. Transl Psychiatry. 7:e1086.
Stahl EA, Breen G, Forstner AJ, McQuillin A, Ripke S, Trubetskoy V, et al.; eQTLGen Consortium; BIOS Consortium; Bipolar Disorder Working Group of the Psychiatric Genomics Consortium (2019). Genome-wide association study identifies 30 loci associated with bipolar disorder. Nat Genet. 51:793–803.
Starnawska A, Demontis D, Pen A, Hedemand A, Nielsen AL, Staunstrup NH, et al. (2016). CACNA1C hypermethylation is associated with bipolar disorder. Transl Psychiatry. 6:e831.
Stefanis NC, Hatzimanolis A, Avramopoulos D, Smyrnis N, Evdokimidis I, Stefanis CN, et al. (2013). Variation in psychosis gene ZNF804A is associated with a refined schizotypy phenotype but not neurocognitive performance in a large young male population. Schizophr Bull. 39:1252–1260.
Tao-Cheng JH, Thein S, Yang Y, Reese TS, Gallant PE (2014). Homer is concentrated at the postsynaptic density and does not redistribute after acute synaptic stimulation. Neuroscience. 266:80–90.
Tapia M, Del Puerto A, Puime A, Sánchez-Ponce D, Fronzaroli-Molinieres L, Pallas-Bazarra N, et al. (2013). GSK3 and β-catenin determines functional expression of sodium channels at the axon initial segment. Cell Mol Life Sci. 70:105–120.
Taviaux S, Williams ME, Harpold MM, Nargeot J, Lory P (1997). Assignment of human genes for beta 2 and beta 4 subunits of voltage-dependent Ca 2+ channels to chromosomes 10p12 and 2q22-q23. Hum Genet. 100:151–154.
Taylor S (2018). Association between COMT Val158Met and psychiatric disorders: a comprehensive meta-analysis. Am J Med Genet B Neuropsychiatr Genet. 177:199–210.
Tecelão D, Mendes A, Martins D, Bramon E, Toulopoulou T, Kravariti E, et al. (2018). The impact of psychosis genome-wide associated ZNF804A variation on verbal fluency connectivity. J Psychiatr Res. 98:17–21.
Tecelão D, Mendes A, Martins D, Fu C, Chaddock CA, Picchioni MM, et al. (2019). The effect of psychosis associated CACNA1C , and its epistasis with ZNF804A, on brain function. Genes Brain Behav. 18:e12510.
Tramontina JF, Yates D, Magalhães PV, Trentini C, Sant’anna MK, Fries GR, et al. (2009). Brain-derived neurotrophic factor gene val66met polymorphism and executive functioning in patients with bipolar disorder. Braz J Psychiatry. 31:136–140.
Tseng CJ, Gilbert TM, Catanese MC, Hightower BG, Peters AT, Parmar AJ, et al. (2020). In vivo human brain expression of histone deacetylases in bipolar disorder. Transl Psychiatry. 10:224.
Vacher H, Mohapatra DP, Trimmer JS (2008). Localization and targeting of voltage-dependent ion channels in mammalian central neurons. Physiol Rev. 88:1407–1447.
Vai B, Riberto M, Ghiglino D, Poletti S, Bollettini I, Lorenzi C, et al. (2017a). A 5-HT1Areceptor promoter polymorphism influences fronto-limbic functional connectivity and depression severity in bipolar disorder. Psychiatry Res Neuroimaging. 270:1–7.
Vai B, Riberto M, Poletti S, Bollettini I, Lorenzi C, Colombo C, Benedetti F (2017b). Catechol-O-methyltransferase Val(108/158)Met polymorphism affects fronto-limbic connectivity during emotional processing in bipolar disorder. Eur Psychiatry. 41:53–59.
Voineskos AN, Lerch JP, Felsky D, Tiwari A, Rajji TK, Miranda D, et al. (2011). The ZNF804A gene: characterization of a novel neural risk mechanism for the major psychoses. Neuropsychopharmacology. 36:1871–1878.
Walters JT, Corvin A, Owen MJ, Williams H, Dragovic M, Quinn EM, et al. (2010). Psychosis susceptibility gene ZNF804A and cognitive performance in schizophrenia. Arch Gen Psychiatry. 67:692–700.
Wang F, McIntosh AM, He Y, Gelernter J, Blumberg HP (2011). The association of genetic variation in CACNA1C with structure and function of a frontotemporal system. Bipolar Disord. 13:696–700.
Wessa M, Linke J, Witt SH, Nieratschker V, Esslinger C, Kirsch P, et al. (2010). The CACNA1C risk variant for bipolar disorder influences limbic activity. Mol Psychiatry. 15:1126–1127.
Wheeler NA, Fuss B (2016). Extracellular cues influencing oligodendrocyte differentiation and (re)myelination. Exp Neurol. 283:512–530.
Wu J, Zhu D, Zhang J, Li G, Liu Z, Sun J (2015). Lithium protects against methamphetamine-induced neurotoxicity in PC12 cells via Akt/GSK3β/mTOR pathway. Biochem Biophys Res Commun. 465:368–373.
Zhang X, Bennett V (1998). Restriction of 480/270-kD ankyrin G to axon proximal segments requires multiple ankyrin G-specific domains. J Cell Biol. 142:1571–1581.
Zhang Z, Lindpaintner K, Che R, He Z, Wang P, Yang P, et al. (2009). The Val/Met functional polymorphism in COMT confers susceptibility to bipolar disorder: evidence from an association study and a meta-analysis. J Neural Transm (Vienna). 116:1193–1200.
Zimmerman AJ, Hafez AK, Amoah SK, Rodriguez BA, Dell’Orco M, Lozano E, et al. (2020). A psychiatric disease-related circular RNA controls synaptic gene expression and cognition. Mol Psychiatry. 25:2712–2727.

Auteurs

Delfina Janiri (D)

Department of Neurology, Fondazione Policlinico Universitario Agostino Gemelli IRCCS.
Department of Psychiatry and Neurology, Sapienza University of Rome.

Georgios D Kotzalidis (GD)

NESMOS Department, Sant'Andrea University Hospital, School of Medicine and Psychology, Sapienza University.

Michelangelo di Luzio (M)

Department of Neuroscience, Section of Psychiatry, Università Cattolica del Sacro Cuore, Rome, Italy.

Giulia Giuseppin (G)

Department of Neuroscience, Section of Psychiatry, Università Cattolica del Sacro Cuore, Rome, Italy.

Alessio Simonetti (A)

Department of Psychiatry and Neurology, Sapienza University of Rome.
Menninger Department of Psychiatry and Behavioral Sciences, Baylor College of Medicine, Houston, Texas, USA.

Luigi Janiri (L)

Department of Neuroscience, Section of Psychiatry, Università Cattolica del Sacro Cuore, Rome, Italy.
Department of Psychiatry, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, Rome, Italy.

Gabriele Sani (G)

Department of Neuroscience, Section of Psychiatry, Università Cattolica del Sacro Cuore, Rome, Italy.
Department of Psychiatry, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, Rome, Italy.

Articles similaires

[Redispensing of expensive oral anticancer medicines: a practical application].

Lisanne N van Merendonk, Kübra Akgöl, Bastiaan Nuijen
1.00
Humans Antineoplastic Agents Administration, Oral Drug Costs Counterfeit Drugs

Smoking Cessation and Incident Cardiovascular Disease.

Jun Hwan Cho, Seung Yong Shin, Hoseob Kim et al.
1.00
Humans Male Smoking Cessation Cardiovascular Diseases Female
Humans United States Aged Cross-Sectional Studies Medicare Part C
1.00
Humans Yoga Low Back Pain Female Male

Classifications MeSH