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Inflammatory biomarkers in Alzheimer's disease plasma
Angharad R. Morgan, Samuel Touchard, Claire Leckey and 41 more
Alzheimer's & Dementia · 2019
doi:10.1016/j.jalz.2019.03.007
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.
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Cited by papers we hold 5
- Systemic and central nervous system neuroinflammatory signatures of neuropsychiatric symptoms and related cognitive decline in older people · 2022Not checked
- Impact of HMGB1, RAGE, and TLR4 in Alzheimer’s Disease (AD): From Risk Factors to Therapeutic Targeting · 2020No notice
- The good, the bad, and the opportunities of the complement system in neurodegenerative disease · 2020No notice
- TLR4 Cross-Talk With NLRP3 Inflammasome and Complement Signaling Pathways in Alzheimer's Disease · 2020No notice
- A Path Toward Precision Medicine for Neuroinflammatory Mechanisms in Alzheimer's Disease · 2020No notice
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