Epigenetic Understanding of Gene-Environment Interactions in Psychiatric Disorders: A New Concept of Clinical Genetics

2014 ◽  
pp. 271-288
Keyword(s):  
Psychiatric Disorders ◽  
Clinical Genetics ◽  
Gene Environment

Gene-environment interactions and correlations in psychiatric disorders

2004 ◽  
Vol 6 (2) ◽  
pp. 119-124 ◽  
Author(s):  
Jennifer Y. F. Lau ◽  
Thalia C. Eley
Keyword(s):  
Psychiatric Disorders ◽  
Gene Environment

scholarly journals A NewT. gondiiMouse Model of Gene-Environment Interaction Relevant to Psychiatric Disease

Scientifica ◽  
2018 ◽  
Vol 2018 ◽  
pp. 1-7 ◽  
Author(s):  
Geetha Kannan ◽  
Emese Prandovszky ◽  
Emily Severance ◽  
Robert H. Yolken ◽  
Mikhail V. Pletnikov
Keyword(s):  
Psychiatric Disorders ◽  
Acoustic Startle ◽  
Experimental System ◽  
Dominant Negative ◽  
Psychiatric Disease ◽  
Environment Interaction ◽  
Dependent Manner ◽  
Mechanistic Studies ◽  
Gene Environment Interaction ◽  
Gene Environment

Infection with the protozoan parasite,Toxoplasma gondii(T. gondii), was linked to several psychiatric disorders. The exact mechanisms of a hypothesized contribution ofT. gondiiinfection are poorly understood, and it appears that only a subset of seropositive individuals go on to develop a mental illness, suggesting genetic vulnerability. In order to stimulate mechanistic studies of how exposure toT. gondiicould interact with genetic predisposition to psychiatric disorders, we have generated and characterized a mouse model of chronicT. gondiiinfection in BALB/c mice with inducible forebrain neuronal expression of a C-terminus truncated dominant-negative form of disrupted-in-schizophrenia 1 (DN-DISC1). In this gene-environment interaction (GxE) model, exposing control and DN-DISC1 male and female mice toT. gondiiproduced sex-dependent abnormalities in locomotor activity and prepulse inhibition of the acoustic startle. No genotype- or sex-dependent effects were found on levels of anti-Toxoplasma IgG antibodies or anti-NMDAR or C1q antibodies. Our work demonstrates that a psychiatric genetic risk factor, DN-DISC1, modulates the neurobehavioral effects of chronicT. gondiiinfection in a sex-dependent manner. The presentT. gondiimodel of GxE provides a valuable experimental system for future mechanistic studies and evaluation of new treatments.

scholarly journals The effects of polygenic risk for psychiatric disorders and smoking behaviour on psychotic experiences in UK Biobank

2019 ◽  
Author(s):  
Judit García-González ◽  
Julia Ramírez ◽  
David M. Howard ◽  
Caroline H Brennan ◽  
Patricia B. Munroe ◽  
...  
Keyword(s):  
Psychiatric Disorders ◽  
Genetic Risk ◽  
Maternal Smoking ◽  
Smoking Status ◽  
Smoking Behaviour ◽  
Environment Interaction ◽  
Uk Biobank ◽  
Psychotic Experiences ◽  
Gene Environment Interaction ◽  
Gene Environment

ABSTRACTWhile psychotic experiences are core symptoms of mental health disorders like schizophrenia, they are also reported by 5-10% of the population. Both smoking behaviour and genetic risk for psychiatric disorders have been associated with psychotic experiences, but the interplay between these factors remains poorly understood. We tested whether smoking status, maternal smoking around birth, and number of packs smoked/year were associated with lifetime occurrence of three psychotic experiences phenotypes: delusions (n=2067), hallucinations (n=6689), and any psychotic experience (delusions or hallucinations; n=7803) in 144818 UK Biobank participants. We next calculated polygenic risk scores for schizophrenia (PRSSCZ), major depression (PRSDEP) and attention deficit hyperactivity disorder (PRSADHD) in the UK Biobank participants to assess whether association between smoking and psychotic experiences was attenuated after adjustment of diagnosis of psychiatric disorders and the PRSs. Finally, we investigated whether smoking exacerbates the effects of genetic predisposition on the psychotic phenotypes in gene-environment interaction models. Smoking status, maternal smoking, and number of packs smoked/year were significantly associated with psychotic experiences (p<1.77×10−5). Except for packs smoked/year, effects were attenuated but remained significant after adjustment for diagnosis of psychiatric disorders and PRSs (p<1.99×10−3). Gene-environment interaction models showed the effects of PRSDEP and PRSADHD(but not PRSSCZ) on delusions (but not hallucinations) were significantly greater in current smokers compared to never smokers (p<0.0028). There were no significant gene-environment interactions for maternal smoking nor for number of packs smoked/year. Our results suggest that both genetic risk of psychiatric disorders and smoking status may have independent and synergistic effects on specific types of psychotic experiences.

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