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Decreased IL-8 levels in CSF and serum of AD patients and negative correlation of MMSE and IL-1 β

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ABSTRACT

Background: 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.

Methods: As 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.

Results: CSF 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.

Conclusion: Our 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 material: The online version of this article (doi:10.1186/s12883-016-0707-z) contains supplementary material, which is available to authorized users.

No MeSH data available.


Analysis of IL-1β levels in CSF of stratified patients by MMSE. CSF IL-1β levels inversely correlated with MMSE score. To further analyze this correlation, AD patients were grouped according to their MMSE score and IL-1β levels were compared to age-matched controls. Box plots represent median levels of CSF IL-1β with the box representing the 25th and 75th percentiles of the observed data, the whiskers showing the 5th and 95th percentiles and dots representing outliers. The MMSE (11-18) group IL-1β was significantly increased compared to the other investigated groups (p < 0.05, ANOVA on Ranks, Dunn’s method)
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Fig3: Analysis of IL-1β levels in CSF of stratified patients by MMSE. CSF IL-1β levels inversely correlated with MMSE score. To further analyze this correlation, AD patients were grouped according to their MMSE score and IL-1β levels were compared to age-matched controls. Box plots represent median levels of CSF IL-1β with the box representing the 25th and 75th percentiles of the observed data, the whiskers showing the 5th and 95th percentiles and dots representing outliers. The MMSE (11-18) group IL-1β was significantly increased compared to the other investigated groups (p < 0.05, ANOVA on Ranks, Dunn’s method)

Mentions: We examined the correlations between cytokine CSF and serum levels in AD patients and their MMSE scores as well CSF Aβ42 as and CSF total tau levels as neurodegenerative markers. Only patients with complete biomarker profiles, including CSF Aβ42, CSF total tau and MMSE scores were included in correlation analysis. CSF total tau and CSF Aβ42 showed no statistically significant correlation with CSF IL-1β, CSF IL-8 or CSF TNF-α levels (Table 2). However, we observed a trend towards a correlation between CSF total tau and CSF IL-8 levels (rs = 0.02, p = 0.06). A statistically significant inverse correlation was observed between the CSF IL-1β concentration and the MMSE score (rs = -0.03, p = 0.02). We therefore stratified the AD patient samples by MMSE score into three equal-sized subgroups reflecting very mild, mild and moderate clinical AD stages and found that in the MMSE (11–18) group (moderate AD) IL-1β was significantly increased compared to age-matched controls (p < 0.05) (Fig. 3), while the mild MMSE (≥24) and the mild to moderate MMSE (18–23) showed no statistically significant difference.Table 2


Decreased IL-8 levels in CSF and serum of AD patients and negative correlation of MMSE and IL-1 β
Analysis of IL-1β levels in CSF of stratified patients by MMSE. CSF IL-1β levels inversely correlated with MMSE score. To further analyze this correlation, AD patients were grouped according to their MMSE score and IL-1β levels were compared to age-matched controls. Box plots represent median levels of CSF IL-1β with the box representing the 25th and 75th percentiles of the observed data, the whiskers showing the 5th and 95th percentiles and dots representing outliers. The MMSE (11-18) group IL-1β was significantly increased compared to the other investigated groups (p < 0.05, ANOVA on Ranks, Dunn’s method)
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Related In: Results  -  Collection

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Fig3: Analysis of IL-1β levels in CSF of stratified patients by MMSE. CSF IL-1β levels inversely correlated with MMSE score. To further analyze this correlation, AD patients were grouped according to their MMSE score and IL-1β levels were compared to age-matched controls. Box plots represent median levels of CSF IL-1β with the box representing the 25th and 75th percentiles of the observed data, the whiskers showing the 5th and 95th percentiles and dots representing outliers. The MMSE (11-18) group IL-1β was significantly increased compared to the other investigated groups (p < 0.05, ANOVA on Ranks, Dunn’s method)
Mentions: We examined the correlations between cytokine CSF and serum levels in AD patients and their MMSE scores as well CSF Aβ42 as and CSF total tau levels as neurodegenerative markers. Only patients with complete biomarker profiles, including CSF Aβ42, CSF total tau and MMSE scores were included in correlation analysis. CSF total tau and CSF Aβ42 showed no statistically significant correlation with CSF IL-1β, CSF IL-8 or CSF TNF-α levels (Table 2). However, we observed a trend towards a correlation between CSF total tau and CSF IL-8 levels (rs = 0.02, p = 0.06). A statistically significant inverse correlation was observed between the CSF IL-1β concentration and the MMSE score (rs = -0.03, p = 0.02). We therefore stratified the AD patient samples by MMSE score into three equal-sized subgroups reflecting very mild, mild and moderate clinical AD stages and found that in the MMSE (11–18) group (moderate AD) IL-1β was significantly increased compared to age-matched controls (p < 0.05) (Fig. 3), while the mild MMSE (≥24) and the mild to moderate MMSE (18–23) showed no statistically significant difference.Table 2

View Article: PubMed Central - PubMed

ABSTRACT

Background: It is widely accepted that neuroinflammatory processes play an important role in the pathogenesis of Alzheimer&rsquo;s disease (AD) and high levels of cytokines and chemokines are detected around A&beta; plaques.

Methods: As neuroinflammation is involved in the development and progression of AD, we measured the pro-inflammatory cytokines interleukin 1&beta; (IL-1&beta;), IL-8 and tumor necrosis factor &alpha; (TNF-&alpha;) in serum and cerebrospinal fluid (CSF) samples from 45&nbsp;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.

Results: CSF as well as serum IL-8 levels were found to be significantly lower in AD patients than in controls (p&thinsp;=&thinsp;0.02). A statistically significant inverse correlation was observed between the CSF level of IL-1&beta; and the MMSE score (rs&thinsp;=&thinsp;-0.03, p&thinsp;=&thinsp;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-1&beta; was significantly increased compared to age-matched controls (p&thinsp;&lt;&thinsp;0.05), whereas in the other investigated groups the increase was not statistically significant.

Conclusion: Our 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 material: The online version of this article (doi:10.1186/s12883-016-0707-z) contains supplementary material, which is available to authorized users.

No MeSH data available.