Biomarkers of inflammation increase with tau and neurodegeneration but not with Amyloid-β in a heterogenous clinical cohort

Abstract

Background: neuroinflammation is an integral part of Alzheimer’s disease (AD) pathology. Inflammatory mediators can exacerbate the production of amyloid-β (Aβ), the propagation of tau pathology and neuronal loss.

Objective: to evaluate the relationship between inflammation markers and established markers of AD in a mixed memory clinic cohort.

Methods: 105 cerebrospinal fluid (CSF) samples from a clinical cohort under investigation for cognitive complaints were analyzed. Levels of Aβ42, total tau, and phosphorylated tau were measured as part of the clinical pathway. Analysis of inflammation markers in CSF samples was performed using multiplex immune assays. Participants were grouped according to their Aβ, tau, and neurodegeneration status and the Paris-Lille-Montpellier (PLM) scale was used to assess the likelihood of AD.

Results: from 102 inflammatory markers analyzed, 19 and 23 markers were significantly associated with CSF total tau and phosphorylated tau levels respectively (p 
Conclusion: CSF inflammation markers increase significantly with tau and neurodegeneration, but not with Aβ in this mixed memory clinic cohort. Thus, such markers could become useful for the clinical diagnosis of neurodegenerative disorders alongside the established Aβ and tau measures.

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Identifiers

ORCID for Angus Prosser: orcid.org/0000-0003-2705-1222

ORCID for Christopher Kipps: orcid.org/0000-0002-5205-9712

ORCID for Jessica Teeling: orcid.org/0000-0003-4004-7391

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