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D13 Modulation of resting state brain connectivity highlights potentiality for functional mri biomarkers
  1. Cristina Sánchez-Castañeda1,2,
  2. Francesco de Pasquale2,3,
  3. Chiara Falletta Caravasso2,
  4. Massimo Marano4,5,
  5. Sabrina Maffi4,5,
  6. Simone Migliore4,5,
  7. Umberto Sabatini2,6,
  8. Ferdinando Squitieri4,5
  1. 1Department of Medicine, School of Medicine and Health Sciences, University of Barcelona, IDIBAPS, Neuroscience Institute, Barcelona, Spain
  2. 2Radiology Department, IRCCS Santa Lucia Foundation, Rome, Italy
  3. 3Faculty of Veterinary Medicine, University of Teramo, Italy
  4. 4LIRH Foundation, Rome, Italy
  5. 5IRCSS Casa Sollievo della Sofferenza, Hospital and Mendel Institute of Human Genetics, Rome, Italy
  6. 6Neuroradiology Department, Magna Graecia University, Catanzaro, Italy

Abstract

Background The spatial pattern of atrophy of a disease is related to its functional connectivity structure, mapped by resting-state functional magnetic resonance imaging (fMRI). Increased somatomotor and default mode resting-state networks play key roles in Huntington’s disease pathophysiology.

Objectives To analyse brain functional connectivity in the somatomotor and default mode networks in patients with different Huntington’s disease stages and HTT gene mutation sizes, its relationship with grey matter volume loss, and functional changes after pridopidine treatment.

Methods Ten patients and 10 controls without treatment underwent T1-weighted imaging and resting-state fMRI; four patients were also assessed after 3 months of pridopidine treatment (90 mg/day). The seed-based functional connectivity patterns from the posterior cingulate cortex and the supplementary motor area (SMA), considered cortical hubs of the somatomotor and default mode networks, respectively, were computed. Grey matter volume was measured by FSL voxel-based morphometry.

Results There was decreased grey matter volume in all cortical and subcortical areas involved in the somatomotor network in patients, with preservation of the SMA. Increased somatomotor and default mode network connectivity was seen in patients compared with controls. The volume of the SMA may be dependent on its connectivity. Pridopidine reduced the intensity of these aberrant connexions.

Conclusions Abnormal functional connectivity of the somatomotor and default mode networks was observed in patients with Huntington’s disease, independent of brain atrophy, which may represent a marker of early dysfunction. Pridopidine modulates these netwoks by reducing connectivity. Results suggest that network connectivity may be used to measure response to experimental therapies.

  • Resting State
  • Functional MRI
  • Pridopidine

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