153 research outputs found

    Mine and me: exploring the neural basis of object ownership.

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    Cognition and brain iron deposition in whole grey matter regions and hippocampal subfields

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    ACKNOWLEDGEMENTS We are grateful to the Aberdeen Children of the 1950's (ACONF) subset of Generation Scotland GS:SFHS who took part in the STRADL study, supported and funded by the Wellcome Trust Strategic Award ‘Stratifying Resilience and Depression Longitudinally’ (STRADL) [104036/Z/14/Z]. Generation Scotland received core support from the Chief Scientist Office of the Scottish Government Health Directorates [CZD/16/6] and the Scottish Funding Council [HR03006] and is currently supported by the Wellcome Trust [216767/Z/19/Z]. HS is supported by the Roland Sutton Academic Trust [0076/R/19]. We also thank the STRADL project team. Research Funding Chief Scientist Office. Grant Number: CZD/16/6 Roland Sutton Academic Trust. Grant Number: 0076/R/19 Scottish Funding Council. Grant Number: HR03006 Wellcome Trust. Grant Number: 104036/Z/14/ZPeer reviewedPublisher PD

    Validation and comparison of two automated methods to quantify brain white matter hyperintensities of presumed vascular origin

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    Funding Data collection was funded by grants from the Alzheimer’s Research Trust (now Alzheimer’s Research UK, grant reference: ART/SPG2003B), Alzheimer’s Research UK (grant reference: ARUK-SB2012B-2), the University of Aberdeen Development Trust (grant reference RGB3109) and NHS Grampian and the Chief Scientist’s Office (grant reference: CAF/08/08). JMJW is funded by the University of Aberdeen Development Trust and TauRx Therapeutics Ltd. CP is funded by Royal Surrey County Hospital NHS Foundation Trust. CJM, ADM, and GDW are funded by the Scottish Funding Council.Peer reviewedPublisher PD

    Increased neural response to social rejection in major depression

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    Background: Being a part of community is critical for survival and individuals with major depressive disorder (MDD) have a greater sensitivity to interpersonal stress that makes them vulnerable to future episodes. Social rejection is a critical risk factor for depression and it is said to increase interpersonal stress and thereby impairing social functioning. It is therefore critical to understand the neural correlates of social rejection in MDD. Methods: To this end, we scanned 15 medicated MDD and 17 healthy individuals during a modified cyberball passing game, where participants were exposed to increasing levels of social exclusion. Neural responses to increasing social exclusion were investigated and compared between groups. Results: We showed that compared to controls, MDD individuals exhibited greater amygdala, insula, and ventrolateral prefrontal cortex activation to increasing social exclusion and this correlated negatively with hedonic tone and self-esteem scores across all participants. Conclusions: These preliminary results support the hypothesis that depression is associated with hyperactive response to social rejection. These findings highlight the importance of studying social interactions in depression, as they often lead to social withdrawal and isolation

    Even a little sleepiness influences neural activation and clinical reasoning in novices

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    Funding: This study was funded by a grant from the Scottish Medical EducationResearch Consortium (SMERC). SMERC had no involvement in thestudy design; collection, analysis, and interpretation of data; writing ofthe report; or the decision to submit the report for publication. Acknowledgements: We thank the students who took part in this project, and the Instituteof Education for Medical and Dental Sciences, University of Aber-deen, for supporting this project. We thank the American College ofPhysicians for the questions used in this study. We thank ProfessorCLELANDET AL.7of9&C?JRFѥ1AGCLACѥ0CNMPRQSusan Jamieson, University of Glasgow, for her support at the stageof seeking funding for this work.Peer reviewedPublisher PD

    Neurobiologic Features of Fibromyalgia Are Also Present Among Rheumatoid Arthritis Patients

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    Funding: The study recieved support from Pfizer. The funder had no role in study design, data collection, analysis, decision to publish or preparation of the manuscript. The content is solely the responsibility of the authors. Funding Information Pfizer Aptinyx Cerephex ACKNOWLEDGEMENTS: The authors wish to thank all of the patient volunteers. We also thank Mariella D’Allesandro for supporting recruitment and data collection.Peer reviewedPostprin

    Characterizing the Neurobiological Mechanisms of Action of Exercise and Cognitive–Behavioral Interventions for Rheumatoid Arthritis Fatigue : a magnetic resonance imaging brain study

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    Open Access via the Wiley/JISC agreement Acknowledgements We would like to thank all the investigators from the original LIFT study, including Kathryn Martin, Lorna Aucott, Neeraj Dhaun, Emma Dures, Stuart R. Gray, Elizabeth Kidd, Vinod Kumar, Karina Lovell, Graeme MacLennan, Paul McNamee, John Norrie, Lorna Paul, Jon Packham, Stefan Siebert, Alison Wearden, and Gary Macfarlane, without whose work this research would not be possible. Furthermore, we thank all the participants who generously supported the LIFT trial. We also acknowledge the contribution of the Trial Steering Committee and Data Monitoring Committee, and Brian Taylor and Mark Forrest (Centre for Healthcare Randomised Trials [CHaRT], University of Aberdeen, Aberdeen, UK) for their technical assistance Funding This study was funded by the Chief Scientist Office (TCS/17/14) and Versus Arthritis (22092).Peer reviewe

    Characterising the neurobiological mechanisms of action of exercise and cognitive behavioural interventions for rheumatoid arthritis fatigue: an MRI brain study

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    Objective: Chronic fatigue is a major clinical unmet need among patients with rheumatoid arthritis (RA). Current therapies are limited to nonpharmacological interventions, such as personalized exercise programs (PEPs) and cognitive–behavioral approaches (CBAs); however, most patients still continue to report severe fatigue. To inform more effective therapies, we conducted a magnetic resonance imaging (MRI) brain study of PEPs and CBAs, nested within a randomized controlled trial (RCT), to identify their neurobiological mechanisms of fatigue reduction in RA. Methods: A subgroup of patients with RA (n = 90), participating in an RCT of PEPs and CBAs for fatigue, undertook a multimodal MRI brain scan following randomization to either usual care (UC) alone or in addition to PEPs and CBAs and again after the intervention (six months). Brain regional volumetric, functional, and structural connectivity indices were curated and then computed employing a causal analysis framework. The primary outcome was fatigue improvement (Chalder fatigue scale). Results: Several structural and functional connections were identified as mediators of fatigue improvement in both PEPs and CBAs compared to UC. PEPs had a more pronounced effect on functional connectivity than CBAs; however, structural connectivity between the left isthmus cingulate cortex (L-ICC) and left paracentral lobule (L-PCL) was shared, and the size of mediation effect ranked highly for both PEPs and CBAs (ßAverage = −0.46, SD 0.61; ßAverage = −0.32, SD 0.47, respectively). Conclusion: The structural connection between the L-ICC and L-PCL appears to be a dominant mechanism for how both PEPs and CBAs reduce fatigue among patients with RA. This supports its potential as a substrate of fatigue neurobiology and a putative candidate for future targeting
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