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D23 The effect of cognitive reserve on age of onset and executive functions in huntington’s disease and its neurobiological bases
  1. Clara Garcia-Gorro1,2,
  2. Maria Garau-Rolandi1,2,
  3. Anira Escrichs1,2,
  4. Nadia Rodriguez-Dechicha3,
  5. Saül Martinez-Horta4,
  6. Irene Vaquer3,
  7. Matilde Calopa5,
  8. Jesus Perez4,
  9. Esteban Muñoz6,7,
  10. Pilar Santacruz6,
  11. Jesus M Ruiz8,
  12. Celia Mareca8,
  13. Nuria Caballol9,
  14. Jaime Kulisevsky4,
  15. Susana Subira3,
  16. Ruth de Diego-Balaguer1,2,10,
  17. Estela Camara1,2
  1. 1Cognition and Brain Plasticity Unit, IDIBELL (Institut d’Investigació Biomèdica de Bellvitge), L’Hospitalet de Llobregat (Barcelona), Spain
  2. 2Basic Psychology Department, Universitat de Barcelona, Barcelona, Spain
  3. 3Fundació Sociosanitària de Barcelona. Hospital Duran i Reynals, Hospitalet de Llobregat (Barcelona), Spain
  4. 4Unitat de Trastorns de Moviment. Departament de Neurologia. Hospital de la Santa Creu i Sant Pau, Barcelona, Spain
  5. 5Hospital Universitari de Bellvitge, L’Hospitalet de Llobregat (Barcelona), Spain
  6. 6IDIBAPS (Institut d’Investigacions Biomèdiques August Pi i Sunyer), Barcelona, Spain
  7. 7Hospital Clínic, Barcelona, Spain
  8. 8Hospital Mare de Deu de la Mercè, Barcelona, Spain
  9. 9Hospital de Sant Joan Despí Moisès Broggi, Sant Joan Despí (Barcelona) Spain
  10. 10ICREA (Catalan Institute for Research and Advanced Studies), Barcelona, Spain


Background Although age of onset of Huntington’s disease (HD) is mainly determined by the size of the CAG repeat expansion, other factors may play a role. One potential factor is Cognitive Reserve (CR), as it has been shown in other neurodegenerative disorders and ageing.

Objective The objective of this study is to investigate the effect of CR on age of onset in HD and to examine the neural bases underlying the individual differences in executive function that could be due to the effects of CR in HD.

Methods Thirty-one HD patients completed a CR questionnaire and were scanned using functional magnetic resonance imaging. We analysed the Resting State Executive Control Network (RS-ECN), a novel approach to study the brain areas underlying executive function. The strength of connectivity with this network was calculated voxel-wise. The difference between the theoeretical and estimated age of onset (26 symptomatic-HD) was calculated for each patient.

Results Our results revealed that high levels of CR significantly delayed the appearance of clinical symptoms. Functional connectivity and morphometry analysis showed a brain reorganisation modulated by CR, which changed the connectivity strength in the anterior cingulate cortex, in the left superior parietal cortex (SPC) and slowed the volume loss in the bilateral precuneus and the bilateral caudate. Furthermore, higher strength of connectivity in the left SPC was related to better performance in cognitive flexibility (TMT B-A) and working memory (Backward Digits Span) tasks.

Conclusions These findings provide converging evidence that CR might act as a protective mechanism for the progression of the disease, delaying the onset of symptoms and improving the performance in executive functions by modulating the RS-ECN and slowing brain atrophy.

  • Cognitive reserve
  • age of onset
  • executive functions
  • resting-state fMRI
  • VBM

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