Institution
King's College London
Education•London, United Kingdom•
About: King's College London is a education organization based out in London, United Kingdom. It is known for research contribution in the topics: Population & Mental health. The organization has 43107 authors who have published 113125 publications receiving 4498103 citations. The organization is also known as: King's & KCL.
Papers published on a yearly basis
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16 Jan 2020
TL;DR: This Primer by Lord and colleagues reviews the epidemiology, mechanisms, clinical detection and treatment of autism and identifies the long-term needs of people with autism.
Abstract: Autism spectrum disorder is a construct used to describe individuals with a specific combination of impairments in social communication and repetitive behaviours, highly restricted interests and/or sensory behaviours beginning early in life. The worldwide prevalence of autism is just under 1%, but estimates are higher in high-income countries. Although gross brain pathology is not characteristic of autism, subtle anatomical and functional differences have been observed in post-mortem, neuroimaging and electrophysiological studies. Initially, it was hoped that accurate measurement of behavioural phenotypes would lead to specific genetic subtypes, but genetic findings have mainly applied to heterogeneous groups that are not specific to autism. Psychosocial interventions in children can improve specific behaviours, such as joint attention, language and social engagement, that may affect further development and could reduce symptom severity. However, further research is necessary to identify the long-term needs of people with autism, and treatments and the mechanisms behind them that could result in improved independence and quality of life over time. Families are often the major source of support for people with autism throughout much of life and need to be considered, along with the perspectives of autistic individuals, in both research and practice.
574 citations
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TL;DR: As predicted by the cognitive model, good treatment outcome was related to greater changes in dysfunctional post-traumatic cognitions, however, low educational attainment and low socioeconomic status were related to better outcome.
574 citations
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TL;DR: In this paper, a protein kinase domain (TK) was identified where TK interacts with the zinc-finger protein nbr1 through a mechanically inducible conformation.
Abstract: The giant sarcomeric protein titin contains a protein kinase domain (TK) ideally positioned to sense mechanical load. We identified a signaling complex where TK interacts with the zinc-finger protein nbr1 through a mechanically inducible conformation. Nbr1 targets the ubiquitin-associated p62/SQSTM1 to sarcomeres, and p62 in turn interacts with MuRF2, a muscle-specific RING-B-box E3 ligase and ligand of the transactivation domain of the serum response transcription factor (SRF). Nuclear translocation of MuRF2 was induced by mechanical inactivity and caused reduction of nuclear SRF and repression of transcription. A human mutation in the titin protein kinase domain causes hereditary muscle disease by disrupting this pathway.
574 citations
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Jason L. Stein1, Sarah E. Medland2, Sarah E. Medland3, Alejandro Arias Vasquez4 +234 more•Institutions (61)
TL;DR: In this article, the authors report genome-wide association meta-analyses and replication for mean bilateral hippocampal, total brain and intracranial volumes from a large multinational consortium.
Abstract: Identifying genetic variants influencing human brain structures may reveal new biological mechanisms underlying cognition and neuropsychiatric illness. The volume of the hippocampus is a biomarker of incipient Alzheimer's disease and is reduced in schizophrenia, major depression and mesial temporal lobe epilepsy. Whereas many brain imaging phenotypes are highly heritable, identifying and replicating genetic influences has been difficult, as small effects and the high costs of magnetic resonance imaging (MRI) have led to underpowered studies. Here we report genome-wide association meta-analyses and replication for mean bilateral hippocampal, total brain and intracranial volumes from a large multinational consortium. The intergenic variant rs7294919 was associated with hippocampal volume (12q24.22; N = 21,151; P = 6.70 × 10(-16)) and the expression levels of the positional candidate gene TESC in brain tissue. Additionally, rs10784502, located within HMGA2, was associated with intracranial volume (12q14.3; N = 15,782; P = 1.12 × 10(-12)). We also identified a suggestive association with total brain volume at rs10494373 within DDR2 (1q23.3; N = 6,500; P = 5.81 × 10(-7)).
574 citations
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TL;DR: It is confirmed that glial cell loss and neuronal size reductions occur in the deeper cortical layers in MDD, but no support is provided for the hypothesis that an altered spatial distribution of glia about neurons plays a role in the development of these changes.
Abstract: Reductions in glial cell density and neuronal size have been described recently in major depressive disorder (MDD). Considering the important trophic influence of glia on neurons, we hypothesized that this glial cell deficit is more prominent close to neurons. In this investigation we have characterized neuronal and glia cytoarchitecture in prefrontal area 9 using spatial point pattern techniques and two-dimensional measures of cell size and density. In post-mortem brain tissue of subjects with MDD, schizophrenia, bipolar disorder (BPD), and normal controls (15 subjects per group), we examined the laminar location and size of all neurons and glial nuclei in a 500 microm wide strip of cortex extending from the pia to the grey-white matter border. In MDD, we observed reductions in glial cell density (30%; P = 0.007) in layer 5 and neuronal size (20%; P = 0.003) in layer 6. We also found that glial cell density (34%; P = 0.003) was reduced in layer 5 in schizophrenia, while neuronal size was reduced in layers 5 (14%) (P = 0.006) and 6 (18%; P = 0.007) in BPD. The spatial pattern investigation of neurons and glia demonstrated no alteration in the clustering of glia about neurons between control and patient groups. These findings confirm that glial cell loss and neuronal size reductions occur in the deeper cortical layers in MDD, but provide no support for the hypothesis that an altered spatial distribution of glia about neurons plays a role in the development of these changes.
574 citations
Authors
Showing all 43962 results
Name | H-index | Papers | Citations |
---|---|---|---|
Cyrus Cooper | 204 | 1869 | 206782 |
David Miller | 203 | 2573 | 204840 |
Rob Knight | 201 | 1061 | 253207 |
Mark I. McCarthy | 200 | 1028 | 187898 |
Michael Rutter | 188 | 676 | 151592 |
Eric Boerwinkle | 183 | 1321 | 170971 |
Terrie E. Moffitt | 182 | 594 | 150609 |
Kenneth S. Kendler | 177 | 1327 | 142251 |
John Hardy | 177 | 1178 | 171694 |
Dorret I. Boomsma | 176 | 1507 | 136353 |
Barry Halliwell | 173 | 662 | 159518 |
Feng Zhang | 172 | 1278 | 181865 |
Simon Baron-Cohen | 172 | 773 | 118071 |
Phillip A. Sharp | 172 | 614 | 117126 |
Yang Yang | 171 | 2644 | 153049 |