Role of cognitive reserve on cognitive function and regional brain atrophy in multiple sclerosis: a two-year longitudinal study
Author(s): ,
M.A Rocca
Affiliations:
Division of Neuroscience, Ospedale San Raffaele - Vita-Salute San Raffaele University
,
P Del Sette
Affiliations:
Neuroimaging Research Unit, INSPE, San Raffaele Scientific Institute
,
G Riccitelli
Affiliations:
Neuroimaging Research Unit, INSPE, San Raffaele Scientific Institute
,
E Pagani
Affiliations:
Neuroimaging Research Unit, INSPE, San Raffaele Scientific Institute
,
P Preziosa
Affiliations:
Neuroimaging Research Unit, INSPE, San Raffaele Scientific Institute
,
V Martinelli
Affiliations:
Dept. of Neurology, San Raffaele Scientific Institute, Vita-Salute San Raffaele University, Milan, Italy
,
G Comi
Affiliations:
Dept. of Neurology, San Raffaele Scientific Institute, Vita-Salute San Raffaele University, Milan, Italy
,
A Falini
Affiliations:
Dept. of Neurology, San Raffaele Scientific Institute, Vita-Salute San Raffaele University, Milan, Italy
M Filippi
Affiliations:
Neuroimaging Research Unit, INSPE, San Raffaele Scientific Institute
ECTRIMS Online Library. Rocca M. 09/16/16; 145717; P1033
Dr. Maria Assunta Rocca
Dr. Maria Assunta Rocca
Contributions
Abstract

Abstract: P1033

Type: Poster

Abstract Category: Pathology and pathogenesis of MS - Imaging

Background: The cognitive reserve (CR) hypothesis states that enriching experiences protect against dementia and cognitive decline. Its protective role against cognitive decline over time in MS is unclear.

Aims. We investigated the predictive role of CR on cognitive decline and gray matter (GM) and white matter (WM) volume changes in MS patients.

Methods: 3D T1-weighted scans and Rao"s Brief Repeatable Battery were obtained from 54 MS patients and 20 healthy controls (HC) at baseline and after two years (median=2.2 years) of follow-up (FU). A reliable change index (RCI) was calculated to assess cognitive decline. A cognitive reserve index (CRI) was calculated including education, intelligence quotient and leisure activities. Regional GM atrophy was estimated using voxel-based-morphometry, whereas longitudinal GM changes were investigated using tensor-based-morphometry analysis. Between group-comparisons (SPM12) and linear regression analysis (SPSS22) were performed to evaluate the effect of CRI on cognitive performance and GM changes, controlling for demographic, clinical and structural MRI measures.

Results: At baseline, higher CRI predicted better performances at information processing speed (IPS) (β=0.30 p=0.02), verbal memory (β=0.43 p=0.001; β=0.52 p< 0.001; β=0.29 p=0.021) and fluency tests (β=0.51 p< 0.001). Compared to HC, MS patients had GM atrophy of the deep GM nuclei, fronto-temporal-parietal-occipital regions, and left (L) cerebellum. Controlling for atrophy within the previous regions, higher CRI predicted better performances at verbal memory (β=0.45 p=0.001; β=0.52 p< 0.001; β=0.29 p=0.021), attention (β=0.28 p=0.002), IPS (β=0.29 p=0.03) and verbal fluency (β=0.38 p=0.003) functions. An interaction between CRI and GM volume in the right (R) superior temporal gyrus, L lingual gyrus and L cerebellum predicted better performances respectively at IPS (β=0.30 p=0.02), verbal fluency (β=0.39 p=0.002) and attention (β=0.30 p=0.01) tests. CRI predicted GM volume in bilateral lingual gyrus (L: β=0.37 p=0.006; R: β=0.27 p=0.05). At FU, cognitive decline was predicted by GM atrophy of several fronto-temporal areas and L cerebellum, while no effect of CRI on cognitive and longitudinal structural changes was found.

Conclusions: CR in MS patients has a protective role on cognitive performance reducing the effect of GM atrophy on cognitive functions. This protective role might lose his efficacy with the progression of disease.

Disclosure: This study has been partially supported by grants from FISM (FISM 2014/R/7 and FISM2013/S/1). M.A. Rocca received speakers honoraria from Biogen Idec, Novartis and ExceMed and receives research support from the Italian Ministry of Health and Fondazione Italiana Sclerosi Multipla.

P. Del Sette has nothing to disclose

G. Riccitelli has nothing to disclose

E. Pagani has nothing to disclose

P. Preziosa has nothing to disclose

V. Martinelli has received honoraria and travel reimbursement for lectures at Meetings and Congresses from Teva Pharma, Bayer, Genzyme, Biogen Idec, Novartis and Merck Serono; he has received research support from Merck Serono and has served as a member in Advisory Board for Bayer, Genzyme, Biogen Idec, Novartis and Merck Serono.

G. Comi has received consulting fees for participating on advisory boards from Novartis, Teva Pharmaceutical Ind. Ltd, Sanofi, Genzyme, Merck Serono, Bayer, Actelion and honorarium for speaking activities for Novartis, Teva Pharmaceutical Ind. Ltd, Sanofi, Genzyme, Merck Serono, Bayer, Biogen, Excemed.

A. Falini has nothing to disclose

M. Filippi is Editor-in-Chief of the Journal of Neurology; serves on scientific advisory board for Teva Pharmaceutical Industries; has received compensation for consulting services and/or speaking activities from Biogen Idec, Excemed, Novartis, and Teva Pharmaceutical Industries; and receives research support from Biogen Idec, Teva Pharmaceutical Industries, Novartis, Italian Ministry of Health, Fondazione Italiana Sclerosi Multipla, Cure PSP, Alzheimer´s Drug Discovery Foundation (ADDF), the Jacques and Gloria Gossweiler Foundation (Switzerland), and ARiSLA (Fondazione Italiana di Ricerca per la SLA).

Abstract: P1033

Type: Poster

Abstract Category: Pathology and pathogenesis of MS - Imaging

Background: The cognitive reserve (CR) hypothesis states that enriching experiences protect against dementia and cognitive decline. Its protective role against cognitive decline over time in MS is unclear.

Aims. We investigated the predictive role of CR on cognitive decline and gray matter (GM) and white matter (WM) volume changes in MS patients.

Methods: 3D T1-weighted scans and Rao"s Brief Repeatable Battery were obtained from 54 MS patients and 20 healthy controls (HC) at baseline and after two years (median=2.2 years) of follow-up (FU). A reliable change index (RCI) was calculated to assess cognitive decline. A cognitive reserve index (CRI) was calculated including education, intelligence quotient and leisure activities. Regional GM atrophy was estimated using voxel-based-morphometry, whereas longitudinal GM changes were investigated using tensor-based-morphometry analysis. Between group-comparisons (SPM12) and linear regression analysis (SPSS22) were performed to evaluate the effect of CRI on cognitive performance and GM changes, controlling for demographic, clinical and structural MRI measures.

Results: At baseline, higher CRI predicted better performances at information processing speed (IPS) (β=0.30 p=0.02), verbal memory (β=0.43 p=0.001; β=0.52 p< 0.001; β=0.29 p=0.021) and fluency tests (β=0.51 p< 0.001). Compared to HC, MS patients had GM atrophy of the deep GM nuclei, fronto-temporal-parietal-occipital regions, and left (L) cerebellum. Controlling for atrophy within the previous regions, higher CRI predicted better performances at verbal memory (β=0.45 p=0.001; β=0.52 p< 0.001; β=0.29 p=0.021), attention (β=0.28 p=0.002), IPS (β=0.29 p=0.03) and verbal fluency (β=0.38 p=0.003) functions. An interaction between CRI and GM volume in the right (R) superior temporal gyrus, L lingual gyrus and L cerebellum predicted better performances respectively at IPS (β=0.30 p=0.02), verbal fluency (β=0.39 p=0.002) and attention (β=0.30 p=0.01) tests. CRI predicted GM volume in bilateral lingual gyrus (L: β=0.37 p=0.006; R: β=0.27 p=0.05). At FU, cognitive decline was predicted by GM atrophy of several fronto-temporal areas and L cerebellum, while no effect of CRI on cognitive and longitudinal structural changes was found.

Conclusions: CR in MS patients has a protective role on cognitive performance reducing the effect of GM atrophy on cognitive functions. This protective role might lose his efficacy with the progression of disease.

Disclosure: This study has been partially supported by grants from FISM (FISM 2014/R/7 and FISM2013/S/1). M.A. Rocca received speakers honoraria from Biogen Idec, Novartis and ExceMed and receives research support from the Italian Ministry of Health and Fondazione Italiana Sclerosi Multipla.

P. Del Sette has nothing to disclose

G. Riccitelli has nothing to disclose

E. Pagani has nothing to disclose

P. Preziosa has nothing to disclose

V. Martinelli has received honoraria and travel reimbursement for lectures at Meetings and Congresses from Teva Pharma, Bayer, Genzyme, Biogen Idec, Novartis and Merck Serono; he has received research support from Merck Serono and has served as a member in Advisory Board for Bayer, Genzyme, Biogen Idec, Novartis and Merck Serono.

G. Comi has received consulting fees for participating on advisory boards from Novartis, Teva Pharmaceutical Ind. Ltd, Sanofi, Genzyme, Merck Serono, Bayer, Actelion and honorarium for speaking activities for Novartis, Teva Pharmaceutical Ind. Ltd, Sanofi, Genzyme, Merck Serono, Bayer, Biogen, Excemed.

A. Falini has nothing to disclose

M. Filippi is Editor-in-Chief of the Journal of Neurology; serves on scientific advisory board for Teva Pharmaceutical Industries; has received compensation for consulting services and/or speaking activities from Biogen Idec, Excemed, Novartis, and Teva Pharmaceutical Industries; and receives research support from Biogen Idec, Teva Pharmaceutical Industries, Novartis, Italian Ministry of Health, Fondazione Italiana Sclerosi Multipla, Cure PSP, Alzheimer´s Drug Discovery Foundation (ADDF), the Jacques and Gloria Gossweiler Foundation (Switzerland), and ARiSLA (Fondazione Italiana di Ricerca per la SLA).

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