• Mult. Scler. · Mar 2019

    Cognitive reserve, cognition, and regional brain damage in MS: A 2 -year longitudinal study.

    • Maria Assunta Rocca, Gianna C Riccitelli, Alessandro Meani, Elisabetta Pagani, Paola Del Sette, Vittorio Martinelli, Giancarlo Comi, Andrea Falini, and Massimo Filippi.
    • Neuroimaging Research Unit, Institute of Experimental Neurology, Division of Neuroscience, San Raffaele Scientific Institute, Vita-Salute San Raffaele University, Milan, Italy/Department of Neurology, Institute of Experimental Neurology, San Raffaele Scientific Institute, Vita-Salute San Raffaele University, Milan, Italy.
    • Mult. Scler. 2019 Mar 1; 25 (3): 372-381.

    BackgroundAccording to the cognitive reserve (CR) theory, enriching experiences protect against cognitive decline.ObjectivesTo investigate the dynamic interaction between CR and global/regional measures of brain white matter (WM) and gray matter (GM) damage and their effect on cognitive performance in multiple sclerosis (MS).MethodsBaseline and 2 -year three-dimensional (3D) T1-weighted scans were obtained from 54 MS patients and 20 healthy controls. Patients' cognitive functions were tested and a cognitive reserve index (CRI) was calculated. Baseline regional atrophy and longitudinal volume changes were investigated using voxel-wise methods. Structural damage and CRI effects on cognitive performance were explored with linear models.ResultsAt baseline, MS patients showed atrophy of the deep GM nuclei, GM/WM frontal-temporal-parietal-occipital regions, and left cerebellum. Controlling for atrophy, higher CRI explained significant portions of variance in verbal memory and verbal fluency (∆ R2 = 0.07-0.16; p < 0.03). The interaction between thalamic volume and CRI was significant (∆ R2 = 0.05; p = 0.03). Longitudinal changes in memory and attention performance were associated with local/global variations of GM/WM and T2 lesions. CRI had no effect on longitudinal cognitive changes.ConclusionIn MS, CR may have a protective role in preserving cognitive functions, moderating the effect of structural damage on cognitive performance. This protective role may diminish with disease progression.

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