Abstract
BackgroundIt is widely accepted that neuroinflammatory processes play an important role in the pathogenesis of Alzheimer’s disease (AD) and high levels of cytokines and chemokines are detected around Aβ plaques.MethodsAs neuroinflammation is involved in the development and progression of AD, we measured the pro-inflammatory cytokines interleukin 1β (IL-1β), IL-8 and tumor necrosis factor α (TNF-α) in serum and cerebrospinal fluid (CSF) samples from 45 AD patients and 53 age-matched control subjects using a highly sensitive multiplex electrochemiluminescence assay. To address the association with disease progression we correlated cognitive status with cytokine levels.ResultsCSF as well as serum IL-8 levels were found to be significantly lower in AD patients than in controls (p = 0.02). A statistically significant inverse correlation was observed between the CSF level of IL-1β and the MMSE score (rs = -0.03, p = 0.02). We therefore stratified the AD patients by their MMSE scores into three equal groups and found that in the AD group with the most severe cognitive impairment CSF-IL-1β was significantly increased compared to age-matched controls (p < 0.05), whereas in the other investigated groups the increase was not statistically significant.ConclusionOur results confirm data suggesting that cytokine alterations are involved in AD pathogenesis and may be helpful as a biomarker for monitoring disease progression.Electronic supplementary materialThe online version of this article (doi:10.1186/s12883-016-0707-z) contains supplementary material, which is available to authorized users.
Highlights
It is widely accepted that neuroinflammatory processes play an important role in the pathogenesis of Alzheimer’s disease (AD) and high levels of cytokines and chemokines are detected around Aβ plaques
interleukin 1β (IL-1β) were found to be elevated in cerebrospinal fluid (CSF), plasma samples or post-mortem brain tissue of AD patients [16,17,18,19], while other studies reported no changes in IL-1β in serum or CSF of AD patients compared to controls [20, 21]
Regarding AD, the above-mentioned IL-1β as well as IL-6, IL-8, IL-10, IL-12, tumor necrosis factor (TNF)-α and transforming growth factor (TGF)-β have been intensively studied in post-mortem brain tissue, serum and CSF samples
Summary
It is widely accepted that neuroinflammatory processes play an important role in the pathogenesis of Alzheimer’s disease (AD) and high levels of cytokines and chemokines are detected around Aβ plaques. Regarding AD, the above-mentioned IL-1β as well as IL-6, IL-8, IL-10, IL-12, tumor necrosis factor (TNF)-α and transforming growth factor (TGF)-β have been intensively studied in post-mortem brain tissue, serum and CSF samples (reviewed in [22,23,24]). Many of these studies, are limited by test cohort sample size and methodological differences analyzing only post-mortem brain tissue, serum or CSF. The results of different studies are often inconsistent and correlations between clinical variables such as mini-mental state examination (MMSE) and cytokine levels in AD patients are often missing
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