scholarly journals A mega-analysis of genome-wide association studies for major depressive disorder

2012 ◽  
Vol 18 (4) ◽  
pp. 497-511 ◽  
Author(s):  
Keyword(s):  
Major Depressive Disorder ◽  
Depressive Disorder ◽  
Association Studies ◽  
Genome Wide Association ◽  
Genome Wide Association Studies ◽  
Major Depressive ◽  
Genome Wide

scholarly journals Meta-analysis of Genome-wide Association Studies for Neuroticism, and the Polygenic Association With Major Depressive Disorder

2015 ◽  
Vol 72 (7) ◽  
pp. 642 ◽  
Author(s):  
Marleen H. M. de Moor ◽  
Stéphanie M. van den Berg ◽  
Karin J. H. Verweij ◽  
Robert F. Krueger ◽  
Michelle Luciano ◽  
...  
Keyword(s):  
Major Depressive Disorder ◽  
Depressive Disorder ◽  
Association Studies ◽  
Meta Analysis ◽  
Genome Wide Association ◽  
Genome Wide Association Studies ◽  
Major Depressive ◽  
Genome Wide

Genome-wide association studies of placebo and duloxetine response in major depressive disorder

2017 ◽  
Vol 18 (3) ◽  
pp. 406-412 ◽  
Author(s):  
M Maciukiewicz ◽  
V S Marshe ◽  
A K Tiwari ◽  
T M Fonseka ◽  
N Freeman ◽  
...  
Keyword(s):  
Major Depressive Disorder ◽  
Depressive Disorder ◽  
Association Studies ◽  
Genome Wide Association ◽  
Genome Wide Association Studies ◽  
Major Depressive ◽  
Genome Wide

scholarly journals Systems Approach to Identify Common Genes and Pathways Associated with Response to Selective Serotonin Reuptake Inhibitors and Major Depression Risk

2019 ◽  
Vol 20 (8) ◽  
pp. 1993 ◽  
Author(s):  
Ankit Srivastava ◽  
Priyanka Singh ◽  
Hitesh Gupta ◽  
Harpreet Kaur ◽  
Neha Kanojia ◽  
...  
Keyword(s):  
Major Depressive Disorder ◽  
Depressive Disorder ◽  
Association Studies ◽  
Gene Set Enrichment Analysis ◽  
Genome Wide Association ◽  
Genome Wide Association Studies ◽  
Antidepressant Response ◽  
Major Depressive ◽  
Disease Etiology ◽  
Genome Wide

Despite numerous studies on major depressive disorder (MDD) susceptibility, the precise underlying molecular mechanism has not been elucidated which restricts the development of etiology-based disease-modifying drug. Major depressive disorder treatment is still symptomatic and is the leading cause of (~30%) failure of the current antidepressant therapy. Here we comprehended the probable genes and pathways commonly associated with antidepressant response and MDD. A systematic review was conducted, and candidate genes/pathways associated with antidepressant response and MDD were identified using an integrative genetics approach. Initially, single nucleotide polymorphisms (SNPs)/genes found to be significantly associated with antidepressant response were systematically reviewed and retrieved from the candidate studies and genome-wide association studies (GWAS). Also, significant variations concerning MDD susceptibility were extracted from GWAS only. We found 245 (Set A) and 800 (Set B) significantly associated genes with antidepressant response and MDD, respectively. Further, gene set enrichment analysis revealed the top five co-occurring molecular pathways (p ≤ 0.05) among the two sets of genes: Cushing syndrome, Axon guidance, cAMP signaling pathway, Insulin secretion, and Glutamatergic synapse, wherein all show a very close relation to synaptic plasticity. Integrative analyses of candidate gene and genome-wide association studies would enable us to investigate the putative targets for the development of disease etiology-based antidepressant that might be more promising than current ones.

scholarly journals The genetics of the mood disorder spectrum: genome-wide association analyses of over 185,000 cases and 439,000 controls

2018 ◽  
Author(s):  
Jonathan R. I. Coleman ◽  
Héléna A. Gaspar ◽  
Julien Bryois ◽  
Gerome Breen ◽  
◽  
...  
Keyword(s):  
Bipolar Disorder ◽  
Major Depressive Disorder ◽  
Major Depression ◽  
Depressive Disorder ◽  
Mood Disorders ◽  
Genome Wide Association ◽  
Genome Wide Association Studies ◽  
Major Depressive ◽  
Genome Wide ◽  
Genome Wide Significance

AbstractBackgroundMood disorders (including major depressive disorder and bipolar disorder) affect 10-20% of the population. They range from brief, mild episodes to severe, incapacitating conditions that markedly impact lives. Despite their diagnostic distinction, multiple approaches have shown considerable sharing of risk factors across the mood disorders.MethodsTo clarify their shared molecular genetic basis, and to highlight disorder-specific associations, we meta-analysed data from the latest Psychiatric Genomics Consortium (PGC) genome-wide association studies of major depression (including data from 23andMe) and bipolar disorder, and an additional major depressive disorder cohort from UK Biobank (total: 185,285 cases, 439,741 controls; non-overlapping N = 609,424).ResultsSeventy-three loci reached genome-wide significance in the meta-analysis, including 15 that are novel for mood disorders. More genome-wide significant loci from the PGC analysis of major depression than bipolar disorder reached genome-wide significance. Genetic correlations revealed that type 2 bipolar disorder correlates strongly with recurrent and single episode major depressive disorder. Systems biology analyses highlight both similarities and differences between the mood disorders, particularly in the mouse brain cell types implicated by the expression patterns of associated genes. The mood disorders also differ in their genetic correlation with educational attainment – positive in bipolar disorder but negative in major depressive disorder.ConclusionsThe mood disorders share several genetic associations, and can be combined effectively to increase variant discovery. However, we demonstrate several differences between these disorders. Analysing subtypes of major depressive disorder and bipolar disorder provides evidence for a genetic mood disorders spectrum.

scholarly journals Genome-wide association of major depression: description of samples for the GAIN Major Depressive Disorder Study: NTR and NESDA biobank projects

2008 ◽  
Vol 16 (3) ◽  
pp. 335-342 ◽  
Author(s):  
Dorret I Boomsma ◽  
Gonneke Willemsen ◽  
Patrick F Sullivan ◽  
Peter Heutink ◽  
Piet Meijer ◽  
...  
Keyword(s):  
Major Depressive Disorder ◽  
Major Depression ◽  
Depressive Disorder ◽  
Genome Wide Association ◽  
Major Depressive ◽  
Genome Wide

scholarly journals Relationship between the LHPP Gene Polymorphism and Resting-State Brain Activity in Major Depressive Disorder

2016 ◽  
Vol 2016 ◽  
pp. 1-8 ◽  
Author(s):  
Lingling Cui ◽  
Xiaohong Gong ◽  
Yanqing Tang ◽  
Lingtao Kong ◽  
Miao Chang ◽  
...  
Keyword(s):  
Major Depressive Disorder ◽  
Prefrontal Cortex ◽  
Depressive Disorder ◽  
Resting State ◽  
Brain Activity ◽  
Association Studies ◽  
Neural System ◽  
Middle Temporal Gyrus ◽  
Genome Wide Association Studies ◽  
Major Depressive

A single-nucleotide polymorphism at the LHPP gene (rs35936514) has been reported in genome-wide association studies to be associated with major depressive disorder (MDD). However, the neural system effects of rs35936514 that mediate the association are unknown. The present work explores whether the LHPP rs35936514 polymorphism moderates brain regional activity in MDD. A total of 160 subjects were studied: a CC group homozygous for the C allele (23 individuals with MDD and 57 controls) and a T-carrier group carrying the high risk T allele (CT/TT genotypes; 22 MDD and 58 controls). All participants underwent resting-state functional magnetic resonance imaging (rs-fMRI) scanning. Brain activity was assessed using the amplitudes of low-frequency fluctuations (ALFF). MDD patients showed a significant increased ALFF in the left middle temporal gyrus and occipital cortex. The T-carrier group showed increased ALFF in the left superior temporal gyrus. Significant diagnosis × genotype interaction was noted in the bilateral lingual gyri, bilateral dorsal lateral prefrontal cortex (dlPFC), and left medial prefrontal cortex (mPFC) (P<0.05, corrected). Results demonstrated that MDD patients with LHPP rs35936514 CT/TT genotype may influence the regional brain activity. These findings implicate the effects of the rs35936514 variation on the neural system in MDD.

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