W Cheng; ET Rolls; H Ruan; J Feng Functional Connectivities in the Brain That Mediate the Association Between Depressive Problems and Sleep Quality Journal Article In: JAMA Psychiatry, 2018. Abstract | Links | BibTeX | Tags: 19542, brain, depression, imaging, sleep @article{Cheng2018,
title = {Functional Connectivities in the Brain That Mediate the Association Between Depressive Problems and Sleep Quality},
author = {W Cheng and ET Rolls and H Ruan and J Feng},
url = {https://www.ncbi.nlm.nih.gov/pubmed/30046833},
year = {2018},
date = {2018-07-25},
journal = {JAMA Psychiatry},
abstract = {Importance:
Depression is associated with poor sleep quality. Understanding the neural connectivity that underlies both conditions and mediates the association between them is likely to lead to better-directed treatments for depression and associated sleep problems.
Objective:
To identify the brain areas that mediate the association of depressive symptoms with poor sleep quality and advance understanding of the differences in brain connectivity in depression.
Design, Setting, and Participants:
This study collected data from participants in the Human Connectome Project using the Adult Self-report of Depressive Problems portion of the Achenbach Adult Self-Report for Ages 18-59, a survey of self-reported sleep quality, and resting-state functional magnetic resonance imaging. Cross-validation of the sleep findings was conducted in 8718 participants from the UK Biobank.
Main Outcomes and Measures:
Correlations between functional connectivity, scores on the Adult Self-Report of Depressive Problems, and sleep quality.
Results:
A total of 1017 participants from the Human Connectome Project (of whom 546 [53.7%] were female; age range, 22 to 35 years) drawn from a general population in the United States were included. The Depressive Problems score was positively correlated with poor sleep quality (r = 0.371; P < .001). A total of 162 functional connectivity links involving areas associated with sleep, such as the precuneus, anterior cingulate cortex, and the lateral orbitofrontal cortex, were identified. Of these links, 39 were also associated with the Depressive Problems scores. The brain areas with increased functional connectivity associated with both sleep and Depressive Problems scores included the lateral orbitofrontal cortex, dorsolateral prefrontal cortex, anterior and posterior cingulate cortices, insula, parahippocampal gyrus, hippocampus, amygdala, temporal cortex, and precuneus. A mediation analysis showed that these functional connectivities underlie the association of the Depressive Problems score with poor sleep quality (β = 0.0139; P < .001).
Conclusions and Relevance:
The implication of these findings is that the increased functional connectivity between these brain regions provides a neural basis for the association between depression and poor sleep quality. An important finding was that the Depressive Problems scores in this general population were correlated with functional connectivities between areas, including the lateral orbitofrontal cortex, cingulate cortex, precuneus, angular gyrus, and temporal cortex. The findings have implications for the treatment of depression and poor sleep quality.},
keywords = {19542, brain, depression, imaging, sleep},
pubstate = {published},
tppubtype = {article}
}
Importance:
Depression is associated with poor sleep quality. Understanding the neural connectivity that underlies both conditions and mediates the association between them is likely to lead to better-directed treatments for depression and associated sleep problems.
Objective:
To identify the brain areas that mediate the association of depressive symptoms with poor sleep quality and advance understanding of the differences in brain connectivity in depression.
Design, Setting, and Participants:
This study collected data from participants in the Human Connectome Project using the Adult Self-report of Depressive Problems portion of the Achenbach Adult Self-Report for Ages 18-59, a survey of self-reported sleep quality, and resting-state functional magnetic resonance imaging. Cross-validation of the sleep findings was conducted in 8718 participants from the UK Biobank.
Main Outcomes and Measures:
Correlations between functional connectivity, scores on the Adult Self-Report of Depressive Problems, and sleep quality.
Results:
A total of 1017 participants from the Human Connectome Project (of whom 546 [53.7%] were female; age range, 22 to 35 years) drawn from a general population in the United States were included. The Depressive Problems score was positively correlated with poor sleep quality (r = 0.371; P < .001). A total of 162 functional connectivity links involving areas associated with sleep, such as the precuneus, anterior cingulate cortex, and the lateral orbitofrontal cortex, were identified. Of these links, 39 were also associated with the Depressive Problems scores. The brain areas with increased functional connectivity associated with both sleep and Depressive Problems scores included the lateral orbitofrontal cortex, dorsolateral prefrontal cortex, anterior and posterior cingulate cortices, insula, parahippocampal gyrus, hippocampus, amygdala, temporal cortex, and precuneus. A mediation analysis showed that these functional connectivities underlie the association of the Depressive Problems score with poor sleep quality (β = 0.0139; P < .001).
Conclusions and Relevance:
The implication of these findings is that the increased functional connectivity between these brain regions provides a neural basis for the association between depression and poor sleep quality. An important finding was that the Depressive Problems scores in this general population were correlated with functional connectivities between areas, including the lateral orbitofrontal cortex, cingulate cortex, precuneus, angular gyrus, and temporal cortex. The findings have implications for the treatment of depression and poor sleep quality. |
Qiang Luo; Qiang Chen; Wenjia Wang et al Association of a Schizophrenia-Risk Nonsynonymous Variant With Putamen Volume in Adolescents: A Voxelwise and Genome-Wide Association Study Journal Article In: JAMA Psychiatry, 2018. Abstract | Links | BibTeX | Tags: 19542, genetics, schizophrenia @article{Qiang Luo2018,
title = {Association of a Schizophrenia-Risk Nonsynonymous Variant With Putamen Volume in Adolescents: A Voxelwise and Genome-Wide Association Study},
author = {Qiang Luo and Qiang Chen and Wenjia Wang et al },
url = {https://www.ncbi.nlm.nih.gov/pubmed/30649180},
year = {2018},
date = {2018-01-16},
journal = {JAMA Psychiatry},
abstract = {Importance:
Deviation from normal adolescent brain development precedes manifestations of many major psychiatric symptoms. Such altered developmental trajectories in adolescents may be linked to genetic risk for psychopathology.
Objective:
To identify genetic variants associated with adolescent brain structure and explore psychopathologic relevance of such associations.
Design, Setting, and Participants:
Voxelwise genome-wide association study in a cohort of healthy adolescents aged 14 years and validation of the findings using 4 independent samples across the life span with allele-specific expression analysis of top hits. Group comparison of the identified gene-brain association among patients with schizophrenia, unaffected siblings, and healthy control individuals. This was a population-based, multicenter study combined with a clinical sample that included participants from the IMAGEN cohort, Saguenay Youth Study, Three-City Study, and Lieber Institute for Brain Development sample cohorts and UK biobank who were assessed for both brain imaging and genetic sequencing. Clinical samples included patients with schizophrenia and unaffected siblings of patients from the Lieber Institute for Brain Development study. Data were analyzed between October 2015 and April 2018.
Main Outcomes and Measures:
Gray matter volume was assessed by neuroimaging and genetic variants were genotyped by Illumina BeadChip.
Results:
The discovery sample included 1721 adolescents (873 girls [50.7%]), with a mean (SD) age of 14.44 (0.41) years. The replication samples consisted of 8690 healthy adults (4497 women [51.8%]) from 4 independent studies across the life span. A nonsynonymous genetic variant (minor T allele of rs13107325 in SLC39A8, a gene implicated in schizophrenia) was associated with greater gray matter volume of the putamen (variance explained of 4.21% in the left hemisphere; 8.66; 95% CI, 6.59-10.81; P = 5.35 × 10-18; and 4.44% in the right hemisphere; t = 8.90; 95% CI, 6.75-11.19; P = 6.80 × 10-19) and also with a lower gene expression of SLC39A8 specifically in the putamen (t127 = -3.87; P = 1.70 × 10-4). The identified association was validated in samples across the life span but was significantly weakened in both patients with schizophrenia (z = -3.05; P = .002; n = 157) and unaffected siblings (z = -2.08; P = .04; n = 149).
Conclusions and Relevance:
Our results show that a missense mutation in gene SLC39A8 is associated with larger gray matter volume in the putamen and that this association is significantly weakened in schizophrenia. These results may suggest a role for aberrant ion transport in the etiology of psychosis and provide a target for preemptive developmental interventions aimed at restoring the functional effect of this mutation.},
keywords = {19542, genetics, schizophrenia},
pubstate = {published},
tppubtype = {article}
}
Importance:
Deviation from normal adolescent brain development precedes manifestations of many major psychiatric symptoms. Such altered developmental trajectories in adolescents may be linked to genetic risk for psychopathology.
Objective:
To identify genetic variants associated with adolescent brain structure and explore psychopathologic relevance of such associations.
Design, Setting, and Participants:
Voxelwise genome-wide association study in a cohort of healthy adolescents aged 14 years and validation of the findings using 4 independent samples across the life span with allele-specific expression analysis of top hits. Group comparison of the identified gene-brain association among patients with schizophrenia, unaffected siblings, and healthy control individuals. This was a population-based, multicenter study combined with a clinical sample that included participants from the IMAGEN cohort, Saguenay Youth Study, Three-City Study, and Lieber Institute for Brain Development sample cohorts and UK biobank who were assessed for both brain imaging and genetic sequencing. Clinical samples included patients with schizophrenia and unaffected siblings of patients from the Lieber Institute for Brain Development study. Data were analyzed between October 2015 and April 2018.
Main Outcomes and Measures:
Gray matter volume was assessed by neuroimaging and genetic variants were genotyped by Illumina BeadChip.
Results:
The discovery sample included 1721 adolescents (873 girls [50.7%]), with a mean (SD) age of 14.44 (0.41) years. The replication samples consisted of 8690 healthy adults (4497 women [51.8%]) from 4 independent studies across the life span. A nonsynonymous genetic variant (minor T allele of rs13107325 in SLC39A8, a gene implicated in schizophrenia) was associated with greater gray matter volume of the putamen (variance explained of 4.21% in the left hemisphere; 8.66; 95% CI, 6.59-10.81; P = 5.35 × 10-18; and 4.44% in the right hemisphere; t = 8.90; 95% CI, 6.75-11.19; P = 6.80 × 10-19) and also with a lower gene expression of SLC39A8 specifically in the putamen (t127 = -3.87; P = 1.70 × 10-4). The identified association was validated in samples across the life span but was significantly weakened in both patients with schizophrenia (z = -3.05; P = .002; n = 157) and unaffected siblings (z = -2.08; P = .04; n = 149).
Conclusions and Relevance:
Our results show that a missense mutation in gene SLC39A8 is associated with larger gray matter volume in the putamen and that this association is significantly weakened in schizophrenia. These results may suggest a role for aberrant ion transport in the etiology of psychosis and provide a target for preemptive developmental interventions aimed at restoring the functional effect of this mutation. |
