Alzheimers & Dementia
Author:
Keywords:
Science & Technology, Life Sciences & Biomedicine, Clinical Neurology, Neurosciences & Neurology, Alzheimer's disease, Biomarker, Plasma, Inflammation, Complement, MILD COGNITIVE IMPAIRMENT, NONSTEROIDAL ANTIINFLAMMATORY DRUGS, GENOME-WIDE ASSOCIATION, IMMUNE-SYSTEM, CEREBROSPINAL-FLUID, IDENTIFIES VARIANTS, FACTOR-H, COMPLEMENT, SERUM, RISK, Aged, Alzheimer Disease, Amyloid beta-Peptides, Biomarkers, Cognitive Dysfunction, Cohort Studies, Complement Factor B, Complement Factor H, Humans, Internationality, Prognosis, NIMA Consortium, Annex: NIMA–Wellcome Trust Consortium for Neuroimmunology of Mood Disorders and Alzheimer's Disease, 1103 Clinical Sciences, 1109 Neurosciences, Geriatrics, 3202 Clinical sciences, 3209 Neurosciences, 5202 Biological psychology
Abstract:
INTRODUCTION: Plasma biomarkers for Alzheimer's disease (AD) diagnosis/stratification are a "Holy Grail" of AD research and intensively sought; however, there are no well-established plasma markers. METHODS: A hypothesis-led plasma biomarker search was conducted in the context of international multicenter studies. The discovery phase measured 53 inflammatory proteins in elderly control (CTL; 259), mild cognitive impairment (MCI; 199), and AD (262) subjects from AddNeuroMed. RESULTS: Ten analytes showed significant intergroup differences. Logistic regression identified five (FB, FH, sCR1, MCP-1, eotaxin-1) that, age/APOε4 adjusted, optimally differentiated AD and CTL (AUC: 0.79), and three (sCR1, MCP-1, eotaxin-1) that optimally differentiated AD and MCI (AUC: 0.74). These models replicated in an independent cohort (EMIF; AUC 0.81 and 0.67). Two analytes (FB, FH) plus age predicted MCI progression to AD (AUC: 0.71). DISCUSSION: Plasma markers of inflammation and complement dysregulation support diagnosis and outcome prediction in AD and MCI. Further replication is needed before clinical translation.