Josje Hazen1, Maria Vistnes2,3, Maria L Barca4,5, Rannveig S Eldholm6,7, Karin Persson4,5, Anne Brækhus4,5,6, Ingvild Saltvedt7,8, Geir Selbæk4,9,10, Knut Engedal4,5, Anne-Brita Knapskog5. 1. Faculty of Medicine, University Medical Center Utrecht, Utrecht University, Utrecht, The Netherlands. 2. Department of Internal Medicine, Diakonhjemmet Hospital. 3. Institute for Experimental Medical Research, Oslo University Hospital and University of Oslo. 4. Norwegian National Advisory Unit on Ageing and Health, Vestfold Hospital Trust, Tønsberg. 5. Departments of Geriatric Medicine. 6. Neurology, Oslo University Hospital Ullevaal, Oslo. 7. Department of Neuromedicine and Movement Science, Norwegian University of Science and Technology (NTNU). 8. Department of Geriatrics, St. Olavs Hospital, University Hospital of Trondheim, Trondheim. 9. Centre for Old Age Psychiatric Research, Innlandet Hospital Trust, Ottestad, Norway. 10. Institute of Health and Society, University of Oslo, Oslo.
Abstract
OBJECTIVE: Neuroinflammation may play an important role in the pathogenesis and progression of Alzheimer disease (AD). The aim of the present study was to detect whether increased inflammatory activity at baseline could predict cognitive and functional decline in patients with amnestic mild cognitive impairment (aMCI) or AD dementia after 2 years. METHODS: Serum samples from 242 memory clinic patients with an aMCI (n=88) or AD dementia (n=154) were analyzed for C-reactive protein and for 14 other inflammatory markers [interleukin (IL)-1β, interleukin-1 receptor antagonist, IL-6, IL-10, IL-12p40, IL-17a, IL-18, IL-22, IL-33, tumor necrosis factor, cluster of differentiation 40 ligand, interferon-γ, chemokine ligand (CCL) 2, and CCL4] by bead-based multiplex immunoassay. Disease progression was measured by the annual increase in the Clinical Dementia Rating Scale Sum of Boxes (CDR-SB) and annual decrease in the score on the Mini-Mental State Examination (MMSE). RESULTS: No association between increased levels of the inflammatory markers and change on the CDR-SB or MMSE score was found, but there was a significant difference in baseline IL-6 and interleukin-1 receptor antagonist levels between aMCI and AD dementia groups. CONCLUSION: Increased levels of inflammatory markers were not associated with faster progression as measured by the annual change on the CDR-SB or MMSE score.
OBJECTIVE: Neuroinflammation may play an important role in the pathogenesis and progression of Alzheimer disease (AD). The aim of the present study was to detect whether increased inflammatory activity at baseline could predict cognitive and functional decline in patients with amnestic mild cognitive impairment (aMCI) or AD dementia after 2 years. METHODS: Serum samples from 242 memory clinic patients with an aMCI (n=88) or AD dementia (n=154) were analyzed for C-reactive protein and for 14 other inflammatory markers [interleukin (IL)-1β, interleukin-1 receptor antagonist, IL-6, IL-10, IL-12p40, IL-17a, IL-18, IL-22, IL-33, tumornecrosis factor, cluster of differentiation 40 ligand, interferon-γ, chemokine ligand (CCL) 2, and CCL4] by bead-based multiplex immunoassay. Disease progression was measured by the annual increase in the Clinical Dementia Rating Scale Sum of Boxes (CDR-SB) and annual decrease in the score on the Mini-Mental State Examination (MMSE). RESULTS: No association between increased levels of the inflammatory markers and change on the CDR-SB or MMSE score was found, but there was a significant difference in baseline IL-6 and interleukin-1 receptor antagonist levels between aMCI and AD dementia groups. CONCLUSION: Increased levels of inflammatory markers were not associated with faster progression as measured by the annual change on the CDR-SB or MMSE score.
Authors: Mari Aksnes; Hans Christian D Aass; Ann Tiiman; Lars Terenius; Nenad Bogdanović; Vladana Vukojević; Anne-Brita Knapskog Journal: J Alzheimers Dis Date: 2022 Impact factor: 4.160