Low-Temperature Deformation of Mixed Siliciclastic & Carbonate Fault Rocks of the Copper Creek, Hunter Valley, and McConnell Thrusts

This study analyzes the low-temperature deformation of fault rocks associated thrust faults. Each fault has dominantly carbonate rocks in one wall and dominantly siliciclastic rocks in the other. The rocks from the Hunter Valley and Copper Creek thrusts of the Southern Appalachians, and McConnell thrust of the Canadian Rockies, were analyzed using data extracted at the thin section and SEM scale. The rocks, all of which featured a fine-grained carbonate matrix surrounding larger carbonate and siliciclastic carbonates, all experienced general shearing, but deformed by different deformation mechanisms. The Hunter Valley and McConnell samples showed evidence of cataclasis, diffusive mass transfer, diffusion accommodated grain boundary sliding and, in the case of the Hunter Valley fault rocks dislocation creep. The Copper Creek samples, by contrast, deformed primarily via plastic processes such as diffusion mass transfer and dislocation creep, and showed no evidence of cataclasis. Within the Hunter Valley and McConnell fault rocks, brittle processes such as cataclasis seemed to dominate at the thin section scale but SEM data supported ductile deformation of the fine matrix material. In each case, analysis of fabrics defined by grain orientations found that the rocks were deformed under general shear conditions and moderate convergence angles, although the Hunter Valley rocks showed evidence for a strong simple shear component of strain and relatively low (37° to 48°) while rocks from the Copper Creek and McConnell thrusts experienced roughly equal pure and shear strain components and showed evidence for higher convergence angles (51° to 59° and 61° to 68°, respectively). The findings of this study highlight the complicated nature of fault rock deformation as well as the difficulty of situating fault rocks within schemes of fault rock nomenclature, which are largely genetic in nature

The Impact of Worry on Attention to Threat

Prior research has often linked anxiety to attentional vigilance for threat using the dot probe task, which presents probes in spatial locations that were or were not preceded by a putative threat stimulus. The present study investigated the impact of worry on threat vigilance by administering this task during a worry condition and during a mental arithmetic control condition to 56 undergraduate students scoring in the low normal range on a measure of chronic worry. The worry induction was associated with faster responses than arithmetic to probes in the attended location following threat words, indicating the combined influence of worry and threat in facilitating attention. Within the worry condition, responses to probes in the attended location were faster for trials containing threat words than for trials with only neutral words, whereas the converse pattern was observed for responses to probes in the unattended location. This connection between worry states and attentional capture by threat may be central to understanding the impact of hypervigilance on information processing in anxiety and its disorders

The genetic architecture of the human cerebral cortex

The cerebral cortex underlies our complex cognitive capabilities, yet little is known about the specific genetic loci that influence human cortical structure. To identify genetic variants that affect cortical structure, we conducted a genome-wide association meta-analysis of brain magnetic resonance imaging data from 51,665 individuals. We analyzed the surface area and average thickness of the whole cortex and 34 regions with known functional specializations. We identified 199 significant loci and found significant enrichment for loci influencing total surface area within regulatory elements that are active during prenatal cortical development, supporting the radial unit hypothesis. Loci that affect regional surface area cluster near genes in Wnt signaling pathways, which influence progenitor expansion and areal identity. Variation in cortical structure is genetically correlated with cognitive function, Parkinson’s disease, insomnia, depression, neuroticism, and attention deficit hyperactivity disorder

Novel genetic loci associated with hippocampal volume

The hippocampal formation is a brain structure integrally involved in episodic memory, spatial navigation, cognition and stress responsiveness. Structural abnormalities in hippocampal volume and shape are found in several common neuropsychiatric disorders. To identify the genetic underpinnings of hippocampal structure here we perform a genome-wide association study (GWAS) of 33,536 individuals and discover six independent loci significantly associated with hippocampal volume, four of them novel. Of the novel loci, three lie within genes (ASTN2, DPP4 and MAST4) and one is found 200 kb upstream of SHH. A hippocampal subfield analysis shows that a locus within the MSRB3 gene shows evidence of a localized effect along the dentate gyrus, subiculum, CA1 and fissure. Further, we show that genetic variants associated with decreased hippocampal volume are also associated with increased risk for Alzheimer's disease (rg =-0.155). Our findings suggest novel biological pathways through which human genetic variation influences hippocampal volume and risk for neuropsychiatric illness

The genetic architecture of the human cerebral cortex

INTRODUCTION The cerebral cortex underlies our complex cognitive capabilities. Variations in human cortical surface area and thickness are associated with neurological, psychological, and behavioral traits and can be measured in vivo by magnetic resonance imaging (MRI). Studies in model organisms have identified genes that influence cortical structure, but little is known about common genetic variants that affect human cortical structure. RATIONALE To identify genetic variants associated with human cortical structure at both global and regional levels, we conducted a genome-wide association meta-analysis of brain MRI data from 51,665 individuals across 60 cohorts. We analyzed the surface area and average thickness of the whole cortex and 34 cortical regions with known functional specializations. RESULTS We identified 306 nominally genome-wide significant loci (P < 5 × 10−8) associated with cortical structure in a discovery sample of 33,992 participants of European ancestry. Of the 299 loci for which replication data were available, 241 loci influencing surface area and 14 influencing thickness remained significant after replication, with 199 loci passing multiple testing correction (P < 8.3 × 10−10; 187 influencing surface area and 12 influencing thickness). Common genetic variants explained 34% (SE = 3%) of the variation in total surface area and 26% (SE = 2%) in average thickness; surface area and thickness showed a negative genetic correlation (rG = −0.32, SE = 0.05, P = 6.5 × 10−12), which suggests that genetic influences have opposing effects on surface area and thickness. Bioinformatic analyses showed that total surface area is influenced by genetic variants that alter gene regulatory activity in neural progenitor cells during fetal development. By contrast, average thickness is influenced by active regulatory elements in adult brain samples, which may reflect processes that occur after mid-fetal development, such as myelination, branching, or pruning. When considered together, these results support the radial unit hypothesis that different developmental mechanisms promote surface area expansion and increases in thickness. To identify specific genetic influences on individual cortical regions, we controlled for global measures (total surface area or average thickness) in the regional analyses. After multiple testing correction, we identified 175 loci that influence regional surface area and 10 that influence regional thickness. Loci that affect regional surface area cluster near genes involved in the Wnt signaling pathway, which is known to influence areal identity. We observed significant positive genetic correlations and evidence of bidirectional causation of total surface area with both general cognitive functioning and educational attainment. We found additional positive genetic correlations between total surface area and Parkinson’s disease but did not find evidence of causation. Negative genetic correlations were evident between total surface area and insomnia, attention deficit hyperactivity disorder, depressive symptoms, major depressive disorder, and neuroticism. CONCLUSION This large-scale collaborative work enhances our understanding of the genetic architecture of the human cerebral cortex and its regional patterning. The highly polygenic architecture of the cortex suggests that distinct genes are involved in the development of specific cortical areas. Moreover, we find evidence that brain structure is a key phenotype along the causal pathway that leads from genetic variation to differences in general cognitive function

Novel genetic loci underlying human intracranial volume identified through genome-wide association

Intracranial volume reflects the maximally attained brain size during development, and remains stable with loss of tissue in late life. It is highly heritable, but the underlying genes remain largely undetermined. In a genome-wide association study of 32,438 adults, we discovered five novel loci for intracranial volume and confirmed two known signals. Four of the loci are also associated with adult human stature, but these remained associated with intracranial volume after adjusting for height. We found a high genetic correlation with child head circumference (ρgenetic=0.748), which indicated a similar genetic background and allowed for the identification of four additional loci through meta-analysis (Ncombined = 37,345). Variants for intracranial volume were also related to childhood and adult cognitive function, Parkinson’s disease, and enriched near genes involved in growth pathways including PI3K–AKT signaling. These findings identify biological underpinnings of intracranial volume and provide genetic support for theories on brain reserve and brain overgrowth

Genetic architecture of subcortical brain structures in 38,851 individuals

Subcortical brain structures are integral to motion, consciousness, emotions and learning. We identified common genetic variation related to the volumes of the nucleus accumbens, amygdala, brainstem, caudate nucleus, globus pallidus, putamen and thalamus, using genome-wide association analyses in almost 40,000 individuals from CHARGE, ENIGMA and UK Biobank. We show that variability in subcortical volumes is heritable, and identify 48 significantly associated loci (40 novel at the time of analysis). Annotation of these loci by utilizing gene expression, methylation and neuropathological data identified 199 genes putatively implicated in neurodevelopment, synaptic signaling, axonal transport, apoptosis, inflammation/infection and susceptibility to neurological disorders. This set of genes is significantly enriched for Drosophila orthologs associated with neurodevelopmental phenotypes, suggesting evolutionarily conserved mechanisms. Our findings uncover novel biology and potential drug targets underlying brain development and disease

The genetic architecture of the human cerebral cortex

The cerebral cortex underlies our complex cognitive capabilities, yet little is known about the specific genetic loci that influence human cortical structure. To identify genetic variants that affect cortical structure, we conducted a genome-wide association meta-analysis of brain magnetic resonance imaging data from 51,665 individuals. We analyzed the surface area and average thickness of the whole cortex and 34 regions with known functional specializations. We identified 199 significant loci and found significant enrichment for loci influencing total surface area within regulatory elements that are active during prenatal cortical development, supporting the radial unit hypothesis. Loci that affect regional surface area cluster near genes in Wnt signaling pathways, which influence progenitor expansion and areal identity. Variation in cortical structure is genetically correlated with cognitive function, Parkinson's disease, insomnia, depression, neuroticism, and attention deficit hyperactivity disorder

Low-Temperature Deformation of Mixed Siliciclastic & Carbonate Fault Rocks of the Copper Creek, Hunter Valley, and McConnell Thrusts

This study analyzes the low-temperature deformation of fault rocks associated thrust faults. Each fault has dominantly carbonate rocks in one wall and dominantly siliciclastic rocks in the other. The rocks from the Hunter Valley and Copper Creek thrusts of the Southern Appalachians, and McConnell thrust of the Canadian Rockies, were analyzed using data extracted at the thin section and SEM scale. The rocks, all of which featured a fine-grained carbonate matrix surrounding larger carbonate and siliciclastic carbonates, all experienced general shearing, but deformed by different deformation mechanisms. The Hunter Valley and McConnell samples showed evidence of cataclasis, diffusive mass transfer, diffusion accommodated grain boundary sliding and, in the case of the Hunter Valley fault rocks dislocation creep. The Copper Creek samples, by contrast, deformed primarily via plastic processes such as diffusion mass transfer and dislocation creep, and showed no evidence of cataclasis. Within the Hunter Valley and McConnell fault rocks, brittle processes such as cataclasis seemed to dominate at the thin section scale but SEM data supported ductile deformation of the fine matrix material. In each case, analysis of fabrics defined by grain orientations found that the rocks were deformed under general shear conditions and moderate convergence angles, although the Hunter Valley rocks showed evidence for a strong simple shear component of strain and relatively low (37° to 48°) while rocks from the Copper Creek and McConnell thrusts experienced roughly equal pure and shear strain components and showed evidence for higher convergence angles (51° to 59° and 61° to 68°, respectively). The findings of this study highlight the complicated nature of fault rock deformation as well as the difficulty of situating fault rocks within schemes of fault rock nomenclature, which are largely genetic in nature