scholarly journals Children’s sleep, impulsivity, and anger: shared genetic etiology and implications for developmental psychopathology

2020 ◽  
Vol 61 (10) ◽  
pp. 1070-1079
Author(s):  
Samantha A. Miadich ◽  
Amanda M. Shrewsbury ◽  
Leah D. Doane ◽  
Mary C. Davis ◽  
Sierra Clifford ◽  
...  
2016 ◽  
Author(s):  
Michel G. Nivard ◽  
Suzanne H. Gage ◽  
Jouke J. Hottenga ◽  
Catherina E.M. van Beijsterveldt ◽  
Abdel Abdellaoui ◽  
...  

AbstractVarious non-psychotic psychiatric disorders in childhood and adolescence can precede the onset of schizophrenia, but the nature of this relationship remains unclear. We investigated to what extent the association between schizophrenia and psychiatric disorders in childhood is explained by shared genetic risk factors.Polygenic risk scores (PRS), reflecting an individual’s genetic risk for schizophrenia, were constructed for participants in two birth cohorts (2,588 children from the Netherlands Twin Register (NTR) and 6,127 from the Avon Longitudinal Study of Parents And Children (ALSPAC)). The associations between schizophrenia PRS and measures of anxiety, depression, attention deficit hyperactivity disorder (ADHD), and oppositional defiant disorder/conduct disorder (ODD/CD) were estimated at age 7, 10, 12/13 and 15 years in the two cohorts. Results were then meta-analyzed, and age-effects and differences in the associations between disorders and PRS were formally tested in a meta-regression.The schizophrenia PRS was associated with childhood and adolescent psychopathology Where the association was weaker for ODD/CD at age 7. The associations increased with age this increase was steepest for ADHD and ODD/CD. The results are consistent with a common genetic etiology of schizophrenia and developmental psychopathology as well as with a stronger shared genetic etiology between schizophrenia and adolescent onset psychopathology.A multivariate meta-analysis of multiple and repeated observations enabled to optimally use the longitudinal data across diagnoses in order to provide knowledge on how childhood disorders develop into severe adult psychiatric disorders.


2020 ◽  
Vol 16 (9) ◽  
pp. 1280-1292
Author(s):  
Michael W. Lutz ◽  
Sheng Luo ◽  
Douglas E. Williamson ◽  
Ornit Chiba‐Falek

2017 ◽  
Vol 41 (S1) ◽  
pp. s812-s812 ◽  
Author(s):  
S. Garcia Marin ◽  
I.M. De Haro García ◽  
N. Martínez Pedrosa ◽  
M.D. Ortega García ◽  
V. Marti Garnica

IntroductionIt is well known about relation between skin and mind, not only due to their mutual origin, but also by their illness expression parallelism. We report a case to show that reciprocity.Personal antecedentsWoman, 42-year-old, single. She only suffers from a skin disease; mild psoriasis guttata placed in both elbows and knees. She treated it with local treatment (cortisone cream) during seasonal prutius and the lesions did not grow or expand. She was hospitalized due to psychotic symptoms (paranoid delusions with her colleagues) and started antipsychotics treatment (risperidone 12 mg per day and olanzapine 10 mg per night). By the same time, she suffered a psoriasis crisis. Her psoriatic plaques increased their sizes and her chest and both thighs were affected too. She complained about grave pruritus. All her medical test results were normal. After that, the patient improved her psychotics’ symptoms, but she started with agoraphobic signs and seclusion at home. Psoriasis were even worse than before and she needed metrotexate to treat it. Being introduced to escitalopram 15 mg per day, anxiety and depression symptoms disappeared and her grave psoriasis became the mild one that she knew.ConclusionSchizophrenia was associated with a greater variety of autoimmune diseases than was anticipated. Studies found evidence for a shared genetic etiology between schizophrenia and psoriasis. Despite that, we think that the study of psychopathology can amplify our understanding about the etiopathogenesis of psoriasis and associated mental disorders.Disclosure of interestThe authors have not supplied their declaration of competing interest.


2021 ◽  
Author(s):  
Jill A. Rabinowitz ◽  
Adrian I. Campos ◽  
Jue-Sheng Ong ◽  
Luis M. García-Marín ◽  
Sarael Alcauter ◽  
...  

ABSTRACTGenome-wide association studies (GWAS) have independently identified hundreds of genomic regions associated with brain morphology and substance use. However, the genetic overlap between brain structure and substance use has not been characterized. Here we leverage GWAS summary data of 71 brain imaging measures and alcohol, tobacco, and cannabis use to investigate their genetic overlap using LD score regression. We also used genomic structural equation modeling to model a ‘substance use common genetic factor’ and examined its genetic overlap with brain structure. After accounting for multiple testing, we identified eight significant negative genetic correlations, including between alcoholic drinks per week and average cortical thickness and intracranial volume with the age of smoking initiation; and five positive genetic correlations, including between insula surface area and lifetime cannabis use, and between the common factor with pericalcarine surface area. Our findings highlight a shared genetic etiology between variation in cortical brain morphology and substance use.


Author(s):  
Aldo Córdova-Palomera ◽  
Catherine Tcheandjieu ◽  
Jason Fries ◽  
Paroma Varma ◽  
Vincent S. Chen ◽  
...  

ABSTRACTThe aortic valve is an important determinant of cardiovascular physiology and anatomic location of common human diseases. From a sample of 26,142 European-ancestry participants, we estimated functional aortic valve area by planimetry from prospectively obtained cardiac MRI sequences of the aortic valve. A genome-wide association study of aortic valve area in these UK Biobank participants showed two significant associations indexed by rs71190365 (chr13:50764607, DLEU1, p=1.8×10−9) and rs35991305 (chr12:94191968, CRADD, p=3.4×10−8). From the GWAS findings we constructed a polygenic risk score for aortic valve area, which in a separate cohort of 311,728 individuals without imaging demonstrated that smaller aortic valve area is predictive of increased risk for aortic valve disease (Odds Ratio 0.88, p=2.3×10−6). After excluding subjects with a medical diagnosis of aortic valve stenosis (remaining n=310,546 individuals), phenome-wide association of >10,000 traits showed multiple links between the polygenic score for aortic valve disease and key health-related comorbidities involving the cardiovascular system and autoimmune disease. Genetic correlation analysis supports a shared genetic etiology with between aortic valve size and birthweight along with other cardiovascular conditions. These results illustrate the use of automated phenotyping of cardiac imaging data from the general population to investigate the genetic etiology of aortic valve disease, perform clinical prediction, and uncover new clinical and genetic correlates of cardiac anatomy.


2021 ◽  
pp. 2100199
Author(s):  
Zhaozhong Zhu ◽  
Jiachen Li ◽  
Jiahui Si ◽  
Baoshan Ma ◽  
Huwenbo Shi ◽  
...  

Lung function is a heritable complex phenotype with obesity being one of its important risk factors. However, the knowledge of their shared genetic basis is limited. Most genome-wide association studies (GWASs) for lung function have been based on European populations, limiting the generalisability across populations. Large-scale lung function GWAS in other populations are lacking.We included 100 285 subjects from China Kadoorie Biobank (CKB). To identify novel loci for lung function, single-trait GWAS were performed on FEV1, FVC, FEV1/FVC in CKB. We then performed genome-wide cross-trait analysis between the lung function and obesity traits (body mass index [BMI], BMI-adjusted waist-to-hip ratio, and BMI-adjusted waist circumference) to investigate the shared genetic effects in CKB. Finally, polygenic risk scores (PRSs) of lung function were developed in CKB and its interaction with BMI's association on lung function were examined. We also conducted cross-trait analysis in parallel with CKB using 457 756 subjects from UK Biobank (UKB) for replication and investigation of ancestry specific effect.We identified 9 genome-wide significant novel loci for FEV1, 6 for FVC and 3 for FEV1/FVC in CKB. FEV1 and FVC showed significant negative genetic correlation with obesity traits in both CKB and UKB. Genetic loci shared between lung function and obesity traits highlighted important pathways, including cell proliferation, embryo and tissue development. Mendelian randomisation analysis suggested significant negative causal effect of BMI on FEV1 and on FVC in both CKB and UKB. Lung function PRSs significantly modified the effect of change-in-BMI on change-in-lung function during an average follow-up of 8 years.This large-scale GWAS of lung function identified novel loci and shared genetic etiology between lung function and obesity. Change-in-BMI might affect change-in-lung function differently according to a subject's polygenic background. These findings may open new avenue for the development of molecular-targeted therapies for obesity and lung function improvement.


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