Visual Neuroscience Laboratory, Institute for Biomedical Imaging and Life Sciences (IBILI), Faculty of Medicine, University of Coimbra

Author Of 1 Presentation

Neuropsychology and Cognition Poster Presentation

P0790 - Brain Reserve and Cognitive Reserve on Social Cognition in Multiple Sclerosis: What roles? (ID 1217)

Speakers
Presentation Number
P0790
Presentation Topic
Neuropsychology and Cognition

Abstract

Background

“Classical” cognitive impairment is well characterized in Multiple Sclerosis (MS), but social cognition seems to be an overlooked cognitive domain. The Reserve theory posits that baseline differences in maximal lifetime brain volume (Brain Reserve (BR)) and lifetime intellectual enrichment (Cognitive Reserve (CR)) affect cognitive performance in neurodegenerative disease.

Objectives

To investigate the effects of of BR and CR on social cognition performance, by determining if these factors moderate/attenuate the impact of grey matter (GM) atrophy.

Methods

Sixty MS patients and sixty healthy controls were enrolled. Total intracranial volume (ICV) was used has a proxy of BR and years of formal education as a proxy of CR. All participants underwent Theory of Mind (ToM) testing and 3Tesla brain MRI. Multiple linear regression analyses were performed to assess the protective effect of BR and CR on social cognition (ToM Eyes Test and ToM Videos Test). Furthermore, we investigated differences in effects according to disease duration (<10 years vs >10 years).

Results

In the linear regression analyses investigating the effect of education and ICV on social cognition, cortical GM was the only measure of brain atrophy retained for both ToM Eyes Test (R2 = 0.101, p = 0.017) and Videos Test (R2 = 0.098, p = 0.021), after controlling for age and sex. ICV was also an independent predictor of Eyes Test (R2 = 0.079, p = 0.028) and Videos Test (R2 = 0.097, p = 0.016). Moreover, an ICV x cortical GM volume interaction was significant on Eyes Test (R2 = 0.158, p = 0.002) and Videos Test (R2 = 0.198, p = 0.001), whereby greater ICV attenuated the negative impact of GM atrophy on social cognition tests. Conversely, education was not associated with performance on social cognition tests. Furthermore, stratification for disease duration showed that the protective effect of ICV on social cognition occurred in early stages of disease (<10 years), moderating the impact of GM atrophy. However, this effect was lost in later stages (>10 years).

Conclusions

Social cognition was associated with BR (ICV), which has a moderator effect on the negative impact of GM atrophy, while the CR (education) had no significant effect. Our results support an association between BR and social cognition which is consistent with a strong hereditability of both ICV and social cognition, suggesting that social cognition may be a cognitive domain less influenced by environmental factors, such as CR.

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