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.

The Impact of Prenatal Risk Factors in ADHD: Potential for Gene x Environment Interactions

2009 ◽  
Vol 24 (S1) ◽  
pp. 1-1
Author(s):  
A. Rodriguez
Keyword(s):  
Genetic Predisposition ◽  
Mental Health Problems ◽  
Attention Problems ◽  
Environment Interaction ◽  
Genetic Transmission ◽  
Hyperactivity Disorder ◽  
Gene Environment Interaction ◽  
Gene Environment ◽  
Gene X Environment Interactions ◽  
The Impact

The intrauterine environment is likely to play a key role in the etiology of psychopathology because the brain is particularly sensitive during the entire gestation as it undergoes the most rapid period of development. Neurodevelopmental deficits, such as attention problems, are a manifestation of these brain disturbances, which can in the end be linked to disorders, the most common being Attention Deficit Hyperactivity Disorder (ADHD). Animal models provide strong evidence in support for programming. Human studies present added complexity as genetic predisposition in mothers can increase the risk of e.g. pregnancy smoking or distress, thus, the effect may be carried entirely or in part by genetic transmission. However, neither genes nor environment operate in isolation, but rather in a complex interplay. Although ADHD has been the focus of intense research, little is known about the gene-environment interaction because such studies require very large sample sizes to be sufficiently statistically powered, thus necessitating multi-site collaborations. This presentation covers methodological difficulties associated with gene-environment studies and some of the ways in which our team has tackled these challenges. Data is presented on common maternal lifestyle factors during pregnancy and their relation to mental health problems in children, particularly ADHD, in a backdrop of genetic predisposition.

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 Interaction between CONNEXIN37 and PDE4D gene polymorphisms with susceptibility to ischemic stroke in Chinese population

2019 ◽  
Vol 244 (18) ◽  
pp. 1642-1647
Author(s):  
Lixia Zhang ◽  
Ruohong Ding ◽  
Peng Kuang ◽  
Leiping Wang ◽  
Huixin Deng ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Environment Interaction ◽  
Nucleotide Polymorphisms ◽  
Gene Environment Interaction ◽  
Gene Environment ◽  
Hardy Weinberg Equilibrium ◽  
Never Smokers ◽  
Relationship Of ◽  
Potential Interactions ◽  
The Impact

The objective of this study was to test the relationship of several single nucleotide polymorphisms (SNPs) within phosphodiesterase 4D ( PDE4D) and connexin 37 ( CONNEXIN37) gene additional interactions with ischemic stroke (IS) risk. The online software SNPstats was used for Hardy–Weinberg equilibrium testing. Generalized multifactor dimensionality reduction (GMDR) was employed to detect the potential interactions among CONNEXIN37 gene, PDE4D gene, and smoking. The results indicated that the rs1764391-T and rs966221-G were correlated with higher IS risk, the corresponding ORs (95% CI) were 1.66 (1.21–2.03) and 1.48 (1.11–1.92), respectively. We also found that the first two loci including rs1764391 and rs918592, and the other two-loci including rs1764391 and smoking were significant in the GMDR model. Participants with rs1764391-CT/TT and rs918592-CT/TT genotype have the highest IS risk, compared to subjects with rs1764391-CC and rs918592-CC genotype, OR (95%CI) = 3.16 (1.83–4.45); smokers with rs1764391-CT/TT genotype also have the highest IS risk, compared to never smokers with rs1764391-CC genotype, OR (95%CI) = 2.82 (1.53–4.15), but no significant interaction combinations were found between gene and alcohol drinking. So in this study, the rs1764391-T and rs966221-G, rs1764391–rs918592 interaction, rs1764391–smoking interaction were all associated with higher IS susceptibility. Impact statement Till now, no study investigated the interaction between CONNEXIN37 and PDE4D gene, and the gene–environment interaction. Therefore, in the current study, we aimed to evaluate the impact of interactions between CONNEXIN37 and PDE4D gene, and its interaction with environmental risk factors on susceptibility to ischemic stroke (IS).

Genetic and Epigenetic Models

2019 ◽  
pp. 546-560
Author(s):  
Rudolf Uher
Keyword(s):  
Environmental Exposure ◽  
Genetic Variants ◽  
Current Knowledge ◽  
Environmental Exposures ◽  
Environment Interaction ◽  
Gene Environment Interaction ◽  
Treatment And Prevention ◽  
Gene Environment ◽  
The Individual ◽  
The Impact

Both genetic variation and environmental exposures play key roles in the development of mental health or psychopathology. Their roles are interdependent: The effects of genetic variants depend on environment, and the impact of environment depends on the genetic variants. This chapter will explain and critically review the most important models of gene–environment interplay, including gene–environment correlation, gene–environment interaction, and epigenetics. Gene–environment correlation describes a mechanism where genetic variants influence the likelihood of environmental exposure. Gene–environment interactions refer to a mechanism where genetic variants influence the impact of an environmental exposure on the individual. Finally, epigenetics provides a molecular mechanism through which environmental exposures affect the function of genes for long periods of time. The chapter concludes with a discussion of the limits of current knowledge, its implications for treatment and prevention, and directions for further research.

Sign in / Sign up

Export Citation Format

Share Document