An active cognitive lifestyle as a potential neuroprotective factor in Huntington's disease

Clara Garcia-Gorro, Maria Garau-Rolandi, Anira Escrichs, Nadia Rodriguez-Dechicha, Irene Vaquer, Susana Subira, Matilde Calopa, Saul Martinez-Horta, Jesus Perez-Perez, Jaime Kulisevsky, Esteban Muñoz, Pilar Santacruz, Jesus Ruiz-Idiago, Celia Mareca, Ruth de Diego-Balaguer, Estela Camara

Research output: Contribution to journalArticleResearch

14 Citations (Scopus)


© 2018 Elsevier Ltd A cognitive stimulating lifestyle has been observed to confer cognitive benefits in multiple neurodegenerative diseases. However, the underlying neurobiological basis of this phenomenon remains unclear. Huntington's disease can provide a suitable model to study the effects and neural mechanisms of cognitive engagement in neurodegeneration. In this study, we investigate the effect of lifestyle factors such as education, occupation and engagement in cognitive activities in Huntington's disease gene carriers on cognitive performance and age of onset as well as the underlying neural changes sustaining these effects, measured by magnetic resonance imaging. Specifically, we analyzed both gray matter volume and the strength of connectivity of the executive control resting-state network. High levels of cognitive engagement were significantly associated with more preserved executive functions, a delay in the appearance of symptoms, reduced volume loss of the left precuneus and the bilateral caudate and a modulation of connectivity strength of anterior cingulate cortex and left angular gyrus with the executive control network. These findings suggest that a cognitively stimulating lifestyle may promote brain maintenance by modulating the executive control resting-state network and conferring protection against neurodegeneration, which results in a delayed onset of symptoms and improved performance in executive functions.
Original languageEnglish
Pages (from-to)116-124
Publication statusPublished - 1 Jan 2019


  • Cognitive engagement
  • Executive functions
  • Huntington's disease
  • Neurodegeneration
  • Resting-state fMRI


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