scholarly journals The genetic overlap between mood disorders and cardiometabolic diseases: a systematic review of genome wide and candidate gene studies

2017 ◽  
Vol 7 (1) ◽  
pp. e1007-e1007 ◽  
Author(s):  
A T Amare ◽  
K O Schubert ◽  
M Klingler-Hoffmann ◽  
S Cohen-Woods ◽  
B T Baune
Keyword(s):  
Systematic Review ◽  
Candidate Gene ◽  
Mood Disorders ◽  
Cardiometabolic Diseases ◽  
Genome Wide ◽  
Genetic Overlap ◽  
Candidate Gene Studies

scholarly journals The genetic overlap between mood disorders and cardio-metabolic diseases: A systematic review of genome wide and candidate gene studies

2017 ◽  
Author(s):  
Azmeraw T. Amare ◽  
Klaus Oliver Schubert ◽  
Sarah Cohen-Woods ◽  
Bernhard T. Baune
Keyword(s):  
Candidate Gene ◽  
Mood Disorders ◽  
Metabolic Diseases ◽  
Association Studies ◽  
Lithium Treatment ◽  
Axonal Guidance ◽  
Genome Wide Association Studies ◽  
R Genes ◽  
Genome Wide ◽  
Candidate Gene Studies

ABSTRACTMeta-analyses of genome-wide association studies (meta-GWAS) and candidate gene studies have identified genetic variants associated with cardiovascular diseases, metabolic diseases, and mood disorders. Although previous efforts were successful for individual disease conditions (single disease), limited information exists on shared genetic risk between these disorders. This article presents a detailed review and analysis of cardio-metabolic diseases risk (CMD-R) genes that are also associated with mood disorders. Firstly, we reviewed meta-GWA studies published until January 2016, for the diseases “type 2 diabetes, coronary artery disease, hypertension” and/or for the risk factors “blood pressure, obesity, plasma lipid levels, insulin and glucose related traits”. We then searched the literature for published associations of these CMD-R genes with mood disorders. We considered studies that reported a significant association of at least one of the CMD-R genes and “depressive disorder” OR “depressive symptoms” OR “bipolar disorder” OR “lithium treatment”, OR “serotonin reuptake inhibitors treatment”. Our review revealed 24 potential pleiotropic genes that are likely to be shared between mood disorders and CMD-Rs. These genes include MTHFR, CACNA1D, CACNB2, GNAS, ADRB1, NCAN, REST, FTO, POMC, BDNF, CREB, ITIH4, LEP, GSK3B, SLC18A1, TLR4, PPP1R1B, APOE, CRY2, HTR1A, ADRA2A, TCF7L2, MTNR1B, and IGF1. A pathway analysis of these genes revealed significant pathways: corticotrophin-releasing hormone signaling, AMPK signaling, cAMP-mediated or G-protein coupled receptor signaling, axonal guidance signaling, serotonin and dopamine receptors signaling, dopamine-DARPP32 feedback in cAMP signaling, circadian rhythm signaling and leptin signaling. Our findings provide insights in to the shared biological mechanisms of mood disorders and cardio-metabolic diseases.

scholarly journals Genetic variants related to physical activity or sedentary behaviour: a systematic review

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Lene Aasdahl ◽  
Tom Ivar Lund Nilsen ◽  
Ingebrigt Meisingset ◽  
Anne Lovise Nordstoga ◽  
Kari Anne I. Evensen ◽  
...  
Keyword(s):  
Physical Activity ◽  
Systematic Review ◽  
Candidate Gene ◽  
Sedentary Behaviour ◽  
Genetic Variants ◽  
Candidate Gene Approach ◽  
Genome Wide Association Studies ◽  
High Quality ◽  
Genome Wide ◽  
Candidate Gene Studies

Abstract Background Research shows that part of the variation in physical activity and sedentary behaviour may be explained by genetic factors. Identifying genetic variants associated with physical activity and sedentary behaviour can improve causal inference in physical activity research. The aim of this systematic review was to provide an updated overview of the evidence of genetic variants associated with physical activity or sedentary behaviour. Methods We performed systematic literature searches in PubMed and Embase for studies published from 1990 to April 2020 using keywords relating to “physical activity”, “exercise”, “sedentariness” and “genetics”. Physical activity phenotypes were either based on self-report (e.g., questionnaires, diaries) or objective measures (e.g., accelerometry, pedometer). We considered original studies aiming to i) identify new genetic variants associated with physical activity or sedentary behaviour (i.e., genome wide association studies [GWAS]), or ii) assess the association between known genetic variants and physical activity or sedentary behaviour (i.e., candidate gene studies). Study selection, data extraction, and critical appraisal were carried out by independent researchers, and risk of bias and methodological quality was assessed for all included studies. Results Fifty-four out of 5420 identified records met the inclusion criteria. Six of the included studies were GWAS, whereas 48 used a candidate gene approach. Only one GWAS and three candidate gene studies were considered high-quality. The six GWAS discovered up to 10 single nucleotide polymorphisms (SNPs) associated with physical activity or sedentariness that reached genome-wide significance. In total, the candidate gene studies reported 30 different genes that were associated (p < 0.05) with physical activity or sedentary behaviour. SNPs in or close to nine candidate genes were associated with physical activity or sedentary behaviour in more than one study. Conclusion GWAS have reported up to 10 loci associated with physical activity or sedentary behaviour. Candidate gene studies have pointed to some interesting genetic variants, but few have been replicated. Our review highlights the need for high-quality GWAS in large population-based samples, and with objectively assessed phenotypes, in order to establish robust genetic instruments for physical activity and sedentary behaviour. Furthermore, consistent replications in GWAS are needed to improve credibility of genetic variants. Trial registration Prospero CRD42019119456.

Candidate gene studies of fibromyalgia: a systematic review and meta-analysis

2010 ◽  
Vol 32 (2) ◽  
pp. 417-426 ◽  
Author(s):  
Young Ho Lee ◽  
Sung Jae Choi ◽  
Jong Dae Ji ◽  
Gwan Gyu Song
Keyword(s):  
Systematic Review ◽  
Candidate Gene ◽  
Meta Analysis ◽  
Candidate Gene Studies

scholarly journals Candidate gene studies in gallbladder cancer: A systematic review and meta-analysis

2011 ◽  
Vol 728 (1-2) ◽  
pp. 67-79 ◽  
Author(s):  
Kshitij Srivastava ◽  
Anvesha Srivastava ◽  
Kiran Lata Sharma ◽  
Balraj Mittal
Keyword(s):  
Systematic Review ◽  
Candidate Gene ◽  
Gallbladder Cancer ◽  
Meta Analysis ◽  
Candidate Gene Studies

The Genetic Basis of Addictive Disorders

2017 ◽  
Author(s):  
David Goldman ◽  
Zhifeng Zhou ◽  
Colin Hodgkinson
Keyword(s):  
Candidate Gene ◽  
Effect Size ◽  
Genetic Basis ◽  
Genome Wide Association ◽  
Model Organisms ◽  
Missing Heritability ◽  
Addictive Disorders ◽  
Genome Wide ◽  
Functional Locus ◽  
Candidate Gene Studies

Addictive disorders are moderately to highly heritable, indicating that alleles transmitted from parents are protective, or enhance risk by whatever mechanisms. However, the inheritance of addictive disorders is complex, involving hundreds of genes and variants that are both common and rare, and that vary in effect size and context of action. Genes altering risk for addictions have been identified by pathway and candidate gene studies in humans and model organisms, and genomic approaches including genome-wide association, meiotic linkage, and sequencing. Genes responsible for shared liability to different addictive disorders have been identified, as well as genes that are relatively specific in altering risk of addiction to one agent. An impediment to overarching conclusions is that most of the heritability of addictions is unexplained at the level of gene or functional locus. However, new analytic approaches and tools have created new potentials for resolution of the “missing heritability.”

FC05-01 - Overlap between attention deficit hyperactivity disorder and autism

2011 ◽  
Vol 26 (S2) ◽  
pp. 1834-1834
Author(s):  
M. Fitzgerald
Keyword(s):  
Attention Deficit Hyperactivity Disorder ◽  
Social Interaction ◽  
Candidate Gene ◽  
Attention Deficit ◽  
Clinical Presentation ◽  
Clinical Genetic ◽  
Hyperactivity Disorder ◽  
Pathophysiological Process ◽  
Genome Wide ◽  
Candidate Gene Studies

Objectives/aimsIn this presentation Michael Fitzgerald will investigate the evidence for the clinical, genetic, and other evidence for the overlap between Autism and Attention Deficit Hyperactivity Disorder.MethodsHe will examine the questions of a similar underlying pathophysiological process and alternately a number of pathologies leading to the same clinical presentation. He will examine clinical and epidemiological overlap, overlap mechanisms, deficits in social interaction in Attention Deficit Hyperactivity Disorder, and genome wide gains in Attention Deficit Hyperactivity Disorder and Autism, candidate gene studies as well as neurochemical and treatment issues.ConclusionsThe issue of overlap between ADHD and Autism is being increasingly recognised.

scholarly journals Hypothesis-driven candidate genes for schizophrenia compared to genome-wide association results

2011 ◽  
Vol 42 (3) ◽  
pp. 607-616 ◽  
Author(s):  
A. L. Collins ◽  
Y. Kim ◽  
P. Sklar ◽  
M. C. O'Donovan ◽  
P. F. Sullivan ◽  
...  
Keyword(s):  
Genetic Variation ◽  
Candidate Gene ◽  
Candidate Genes ◽  
Association Studies ◽  
Human Diseases ◽  
Genome Wide Association ◽  
Genome Wide Association Studies ◽  
Common Genetic Variation ◽  
Genome Wide ◽  
Candidate Gene Studies

BackgroundCandidate gene studies have been a key approach to the genetics of schizophrenia (SCZ). However, the results of these studies are confusing and no genes have been unequivocally implicated. The hypothesis-driven candidate gene literature can be appraised by comparison with the results of genome-wide association studies (GWAS).MethodWe describe the characteristics of hypothesis-driven candidate gene studies from the SZGene database, and use pathway analysis to compare hypothesis-driven candidate genes with GWAS results from the International Schizophrenia Consortium (ISC).ResultsSZGene contained 732 autosomal genes evaluated in 1374 studies. These genes had poor statistical power to detect genetic effects typical for human diseases, assessed only 3.7% of genes in the genome, and had low marker densities per gene. Most genes were assessed once or twice (76.9%), providing minimal ability to evaluate consensus across studies. The ISC studies had 89% power to detect a genetic effect typical for common human diseases and assessed 79% of known autosomal common genetic variation. Pathway analyses did not reveal enrichment of smaller ISCpvalues in hypothesis-driven candidate genes, nor did a comprehensive evaluation of meta-hypotheses driving candidate gene selection (SCZ as a disease of the synapse or neurodevelopment). The most studied hypothesis-driven candidate genes (COMT,DRD3,DRD2,HTR2A,NRG1,BDNF,DTNBP1andSLC6A4) had no notable ISC results.ConclusionsWe did not find support for the idea that the hypothesis-driven candidate genes studied in the literature are enriched for the common genetic variation involved in the etiology of SCZ. Larger samples are required to evaluate this conclusion definitively.

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