Journal
JOURNAL OF ALZHEIMERS DISEASE
Volume 49, Issue 4, Pages 1105-1114Publisher
IOS PRESS
DOI: 10.3233/JAD-140669
Keywords
Alzheimer's disease; cognitive decline; complement cascade; cytokine-cytokine receptor interaction; plasma proteins
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Funding
- InnoMed (Innovative Medicines in Europe)
- European Union of the Sixth Framework program priority [FP6-2004-LIFESCIHEALTH-5]
- Alzheimer's Research Trust
- John and Lucille van Geest Foundation
- NIHR Biomedical Research Centre for Mental Health and Biomedical Research Unit for Dementia at the South London
- Maudsley NHS Foundation Trust and Kings College London
- Guy's and St Thomas' Charity
- Maudsley Charity
- Kuopio University Hospital
- UEFBRAIN
- Alzheimers Research UK [ART-PG2010-4] Funding Source: researchfish
- Medical Research Council [G0801464] Funding Source: researchfish
- National Institute for Health Research [NF-SI-0512-10053] Funding Source: researchfish
- Alzheimer"
- s Society [167] Funding Source: researchfish
- MRC [G0801464] Funding Source: UKRI
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Biomarkers of Alzheimer's disease (AD) progression are needed to support the development of urgently needed disease modifying drugs. We employed a SOMAscan assay for quantifying 1,001 proteins in blood samples from 90 AD subjects, 37 stable mild cognitive impaired (MCI) subjects, 39 MCI subjects converting to AD within a year and 69 controls at baseline and one year follow up. We used linear mixed effects models to identify proteins changing significantly over one year with the rate of cognitive decline, which was quantified as the reduction in Mini Mental State Examination (MMSE) scores. Additionally, we investigated proteins changing differently across disease groups and during the conversion from MCI to AD. We found that levels of proteins belonging to the complement cascade increase significantly in fast declining AD patients. Longitudinal changes in the complement cascade might be a surrogate biomarker for disease progression. We also found that members of the cytokine-cytokine receptor interaction pathway change during AD when compared to healthy aging subjects.
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