scholarly journals Gender-Specific Gene–Environment Interaction in Alcohol Dependence: The Impact of Daily Life Events and GABRA2

2013 ◽  
Vol 43 (5) ◽  
pp. 402-414 ◽  
Author(s):  
Brea L. Perry ◽  
Bernice A. Pescosolido ◽  
Kathleen Bucholz ◽  
Howard Edenberg ◽  
John Kramer ◽  
...  
Keyword(s):  
Alcohol Dependence ◽  
Life Events ◽  
Daily Life ◽  
Specific Gene ◽  
Environment Interaction ◽  
Gene Environment Interaction ◽  
Gene Environment ◽  
The Impact ◽  
Gender Specific

scholarly journals Epigenetic Genes and Emotional Reactivity to Daily Life Events: A Multi-Step Gene-Environment Interaction Study

PLoS ONE ◽  
2014 ◽  
Vol 9 (6) ◽  
pp. e100935 ◽  
Author(s):  
Ehsan Pishva ◽  
Marjan Drukker ◽  
Wolfgang Viechtbauer ◽  
Jeroen Decoster ◽  
Dina Collip ◽  
...  
Keyword(s):  
Life Events ◽  
Emotional Reactivity ◽  
Daily Life ◽  
Environment Interaction ◽  
Interaction Study ◽  
Gene Environment Interaction ◽  
Gene Environment

Gene–environment interplay in the etiology of psychosis

2018 ◽  
Vol 48 (12) ◽  
pp. 1925-1936 ◽  
Author(s):  
Alyson Zwicker ◽  
Eileen M. Denovan-Wright ◽  
Rudolf Uher
Keyword(s):  
Environmental Factors ◽  
Genetic Risk ◽  
Environmental Exposures ◽  
Response To Treatment ◽  
Human Potential ◽  
Specific Gene ◽  
Environment Interaction ◽  
Gene Environment ◽  
Increased Risk ◽  
The Impact

AbstractSchizophrenia and other types of psychosis incur suffering, high health care costs and loss of human potential, due to the combination of early onset and poor response to treatment. Our ability to prevent or cure psychosis depends on knowledge of causal mechanisms. Molecular genetic studies show that thousands of common and rare variants contribute to the genetic risk for psychosis. Epidemiological studies have identified many environmental factors associated with increased risk of psychosis. However, no single genetic or environmental factor is sufficient to cause psychosis on its own. The risk of developing psychosis increases with the accumulation of many genetic risk variants and exposures to multiple adverse environmental factors. Additionally, the impact of environmental exposures likely depends on genetic factors, through gene–environment interactions. Only a few specific gene–environment combinations that lead to increased risk of psychosis have been identified to date. An example of replicable gene–environment interaction is a common polymorphism in theAKT1gene that makes its carriers sensitive to developing psychosis with regular cannabis use. A synthesis of results from twin studies, molecular genetics, and epidemiological research outlines the many genetic and environmental factors contributing to psychosis. The interplay between these factors needs to be considered to draw a complete picture of etiology. To reach a more complete explanation of psychosis that can inform preventive strategies, future research should focus on longitudinal assessments of multiple environmental exposures within large, genotyped cohorts beginning early in life.

scholarly journals Could Stress Cause Psychosis in Individuals Vulnerable to Schizophrenia?

CNS Spectrums ◽  
2002 ◽  
Vol 7 (1) ◽  
pp. 33-42 ◽  
Author(s):  
Cheryl Corcoran ◽  
Lilianne Mujica-Parodi ◽  
Scott Yale ◽  
David Leitman ◽  
Dolores Malaspina
Keyword(s):  
Structural Changes ◽  
Time Frame ◽  
Environment Interaction ◽  
Synaptic Remodeling ◽  
Gene Environment Interaction ◽  
Neurodevelopmental Model ◽  
Gene Environment ◽  
Plausible Model ◽  
Neurotoxic Effects ◽  
The Impact

ABSTRACTIt has long been considered that psychosocial stress plays a role in the expression of symptoms in schizophrenia (SZ), as it interacts with latent neural vulnerability that stems from genetic liability and early environmental insult. Advances in the understanding of the neurobiology of the stress cascade in both animal and human studies lead to a plausible model by which this interaction may occur: through neurotoxic effects on the hippocampus that may involve synaptic remodeling. Of late, the neurodevelopmental model of SZ etiology has been favored. But an elaboration of this schema that credits the impact of postnatal events and considers a role for neurodegenerative changes may be more plausible, given the evidence for gene-environment interaction in SZ expression and progressive structural changes observed with magnetic resonance imaging. Furthermore, new insights into nongliotic neurotoxic effects such as apoptosis, failure of neurogenesis, and changes in circuitry lead to an expansion of the time frame in which environmental effects may mediate expression of SZ symptoms.

scholarly journals Shorter Adult Stature Increases the Impact of Risk Factors for Cognitive Impairment: A Comparison of Two Nordic Twin Cohorts

2011 ◽  
Vol 14 (6) ◽  
pp. 544-552 ◽  
Author(s):  
Venla S. Laitala ◽  
Jacob Hjelmborg ◽  
Markku Koskenvuo ◽  
Ismo Räihä ◽  
Juha O. Rinne ◽  
...  
Keyword(s):  
Risk Factors ◽  
Cognitive Impairment ◽  
Cognitive Performance ◽  
Genetic Factors ◽  
Childhood Adversity ◽  
Environment Interaction ◽  
Gene Environment Interaction ◽  
Gene Environment ◽  
The Impact ◽  
Adult Stature

We analyzed the association between mean height and old age cognition in two Nordic twin cohorts with different childhood living conditions. The cognitive performance of 4720 twin individuals from Denmark (mean age 81.6 years, SD = 4.59) and Finland (mean age 74.4 years, SD = 5.26) was measured using validated cognitive screens. Taller height was associated with better cognitive performance in Finland (β-estimates 0.18 SD/10cm, p value < .001, for men and 0.13 SD, p = .008, for women), but this association was not significant in Denmark (β-estimates 0.0093 SD, p value = .16, for men and 0.0075 SD, p value = .016, for women) when adjusted for age and education/social class. Among Finnish participants higher variability of cognitive performance within shorter height quintiles was observed. Analysis using gene-environment interaction models showed that environmental factors exerted a greater impact on cognitive performance in shorter participants, whereas in taller participants' it was explained mainly by genetic factors. Our results suggest that shorter participants with childhood adversity are more vulnerable to environmental risk factors for cognitive impairment.

scholarly journals Issues concerning feedback about genetic testing and risk of depression

2009 ◽  
Vol 194 (5) ◽  
pp. 404-410 ◽  
Author(s):  
Kay Wilhelm ◽  
Bettina Meiser ◽  
Philip B. Mitchell ◽  
Adam W. Finch ◽  
Jennifer E. Siegel ◽  
...  
Keyword(s):  
Serotonin Transporter ◽  
Causal Effect ◽  
Environment Interaction ◽  
Gene Environment Interaction ◽  
Individual Genotype ◽  
Gene Environment ◽  
Serotonin Transporter Genotype ◽  
S Allele ◽  
The Impact

BackgroundRecent studies show that adverse life events have a significantly greater impact on depression onset for those with the s/s allele of the genotype for the 5-HT gene-linked promoter region. Research in genes related to risk of depression leads to the question of how this information is received by individuals.AimsTo investigate factors related to the response to receiving one's own serotonin transporter genotype results.MethodPredictors of the impact of receiving individual genotype data were assessed in 128 participants in a study of gene–environment interaction in depression onset.ResultsTwo-thirds decided to learn their individual genotype results (receivers) and prior to disclosure this decision was associated with a perception of greater benefit from receipt of the information (P=0.001). Receivers completing the 2-week (n=76) and 3-month follow-up (n=78) generally reported feeling pleased with the information and having had a more positive experience than distress. However, distress was related to genotype, with those with the s/s allele being most affected.ConclusionsThere was high interest in, and satisfaction with, learning about one's serotonin transporter genotype. Participants appeared to understand that the gene conferred susceptibility to depression rather than a direct causal effect.

scholarly journals Genetic moderation of environmental risk for depression and anxiety in adolescent girls

2001 ◽  
Vol 179 (2) ◽  
pp. 116-121 ◽  
Author(s):  
Judy Silberg ◽  
Michael Rutter ◽  
Michael Neale ◽  
Lindon Eaves
Keyword(s):  
Life Events ◽  
Structural Equation ◽  
Genetic Factors ◽  
Negative Life Events ◽  
Genetic Effect ◽  
Environment Interaction ◽  
Gene Environment Interaction ◽  
Gene Environment ◽  
Significant Gene ◽  
Independent Life

BackgroundThere is huge individual variation in people's response to negative life events.AimsTo test the hypothesis that genetic factors moderate susceptibility to the environmentally mediated risks associated with negative life events.MethodThe Virginia Twin Study of Adolescent Behavioral Development (VTSABD) was used to study the effects of independent life events (assessed from maternal interview) on depression/anxiety (assessed from child interview) in 184 same-gender female twin pairs, aged 14–17 years, measured on two occasions.ResultsThere was no genetic effect on the independent negative life events studied. A significant gene–environment interaction was found using structural equation modelling. There was no effect of independent life events on adolescents' depression in the absence of parental emotional disorder, but a significant effect in its presence.ConclusionsThere is an environmentally mediated effect of life events on depression/anxiety. Genetic factors play a significant role in individual differences in susceptibility to these environmentally mediated risks.

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