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D21 Longitudinal compensation in the cognitive network in huntington’s disease
  1. Sarah Gregory1,
  2. Stefan Klöppel2,
  3. Jeffrey D Long3,4,
  4. Adeel Razi5,
  5. Elisa Scheller6,
  6. Lora Minkova6,
  7. Alexandra Dürr7,
  8. Raymund AC Roos8,
  9. Blair R Leavitt9,
  10. James A Mills3,
  11. Julie Stout10,
  12. Rachael I Scahill1,
  13. Douglas R Langbehn3,4,
  14. Geraint Rees5,
  15. Sarah J Tabrizi1,
  16. the TrackON investigators
  1. 1Huntington’s Disease Research Group, Institute of Neurology, University College London, London, UK
  2. 2Division Freiburg Brain Imaging, Department of Psychiatry and Psychotherapy and Department of Neurology, Albert-Ludwigs-University Freiburg, University Medical Centre, Freiburg, Germany
  3. 3Department of Psychiatry, Carver College of Medicine, University of Iowa, Iowa, City, IA, USA
  4. 4Department of Biostatistics, College of Public Health, University of Iowa, Iowa, City, IA, USA
  5. 5Wellcome Trust Centre for Neuroimaging, Institute of Neurology, University College London, London, UK
  6. 6Division Freiburg Brain Imaging, Department of Psychiatry and Psychotherapy and Department of Psychology, Laboratory for Biological and Personality Psychology, Albert-Ludwigs-University Freiburg, University Medical Centre, Freiburg, Germany
  7. 7APHP Department of Genetics, Groupe Hospitalier Pitié-Salpêtrière, and Institut du Cerveau et de la Moelle, INSERM U1127, CNRS UMR7225, UPMC Université Paris VI UMR_S1127, Paris, France
  8. 8Leiden University Medical Centre, Department of Neurology, Leiden, The Netherlands
  9. 9Centre for Molecular Medicine and Therapeutics, Department of Medical Genetics, University of British Columbia, Canada
  10. 10School of Psychological Sciences and Institute of Clinical and Cognitive Neuroscience, Monash University, Melbourne, Australia

Abstract

Background In premanifest Huntington’s disease (preHD), disease-related neuronal degeneration is dissociated from the capacity to maintain normal levels of performance during cognitive tasks, which could be explained by compensatory processes. Recently, we devised a novel model of compensation which examined the relationship between disease progression, brain activity and task performance and identified a pattern consistent with asymmetrical compensation in preHD. We now examine the hypotheses that due to changes in neuronal pathology, such compensatory processes will change over time.

Aims To examine possible changes in compensatory processes over time, we extended our cross-sectional model to cover repeated measurements.

Methods Over three annual time points we modelled a) average compensation and b) change in compensation in each case examining the relationships between disease progression using volumetric measures, brain activity using task-based and resting-state fMRI and cognitive task performance.

Results For the average model, we showed weak disease effects centred in the left hemisphere. We also identified a non-significant pattern of asymmetrical compensation consistent with our previous cross-sectional analyses: disease effect in the left hemisphere and compensatory effect in the right. There was, however, very limited evidence of longitudinal change in compensation.

Conclusion While we interpret these findings with considerable caution, they suggest a consistent asymmetrical pattern of compensatory effects. However, the apparent absence of longitudinal change in compensation was more likely due to the fact that interaction models are generally less sensitive to small changes and moreover, the problems that can arise in trying to model compensation per se.

  • Compensation
  • Longitudinal
  • Magnetic Resonance Imaging
  • Asymmetry

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