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Altered cognitive function in systemic lupus erythematosus and associations with inflammation and functional and structural brain changes

Author

Barraclough M1,2, McKie S3, Parker B2,4, Jackson A5, Pemberton P6, Elliott R7, Bruce IN8,2. Ann Rheum Dis. 2019 Apr 12. pii: annrheumdis-2018-214677. doi: 10.1136/annrheumdis-2018-214677. [Epub ahead of print]

Author Information

Arthritis Research UK Centre for Epidemiology, Division of Musculoskeletal and Dermatological Sciences, School of Biological Sciences, Faculty of Biology, Medicine and Health, The University of Manchester, Manchester, UK.

NIHR Manchester Biomedical Research Centre, Manchester University NHS Foundation Trust, Manchester Academic Health Science Centre, Manchester, UK.

FBMH Platform Sciences, Enabling Technologies & Infrastructure, FBMH Research & Innovation, Manchester Academic Health Science Centre, The University of Manchester, Manchester, UK.

Division of Musculoskeletal and Dermatological Sciences, School of Biological Sciences, Faculty ofBiology, Medicine and Health, The University of Manchester, Manchester, UK.

Wolfson Molecular Imaging Centre, Institute of Imaging and Bioinformatics, The University of Manchester, Manchester, UK.

Department of Clinical Biochemistry, Manchester University NHS Foundation Trust, Manchester, UK.

Neuroscience and Psychiatry Unit, Division of Neuroscience and Experimental Psychology, The University of Manchester, Manchester, UK.

Arthritis Research UK Centre for Epidemiology, Division of Musculoskeletal and Dermatological Sciences, School of Biological Sciences, Faculty of Biology, Medicine and Health, The University of Manchester, Manchester, UK ian.bruce@manchester.ac.uk.

Abstract

OBJECTIVES: 

Cognitive dysfunction (CD) is common in systemic lupus erythematosus (SLE) but the cause remains unclear and treatment options are limited. We aimed to compare cognitive function in SLE and healthy controls (HCs) using both behavioural and neuroimaging techniques.

METHODS: 

Patients with SLE with stable disease and HCs were recruited. Clinical and psychological data were collected along with a blood sample for relevant biomarkers. Neurocognitive function was assessed using tests from the Cambridge Neuropsychological Test Automated Battery (CANTAB) and functional magnetic resonance imaging (fMRI) was used to examine brain responses to working memory (WM) and emotional processing (facial emotional recognition task, FERT) tasks.

RESULTS: 

Compared with HCs (n=30), patients with SLE (n=36) scored higher on measures of depression, fatigue and had higher hsCRP (p=0.013), IL-6 (p=0.003) and B lymphocyte stimulator (p<0.001). Patients with SLE had poorer performance on a task of sustained attention (p=0.002) and had altered brain responses, particularly in default mode network (DMN) regions and the caudate, during the WM task. Higher organ damage and higher VCAM-1 were associated with less attenuation of the DMN (p=0.005 and p=0.01, respectively) and lower BOLD signal in the caudate areas (p=0.005 and p=0.001, respectively). Increased IL-6 was also associated with lower BOLD signal in caudate areas (p=0.032).

CONCLUSIONS: 

Sustained attention was impaired in patients with SLE. Poor attenuation of the DMN may contribute to cognitive impairments in SLE and our data suggest that in addition to mood and fatigue inflammatory mechanisms and organ damage impact cognitive functioning in SLE. The multifaceted nature of CD in SLE means any therapeutic interventions should be individually tailored.