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, 5 (3), 424-34
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Alterations of the Neuroinflammatory Markers IL-6 and TRAIL in Alzheimer's Disease

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Alterations of the Neuroinflammatory Markers IL-6 and TRAIL in Alzheimer's Disease

Ya-Ying Wu et al. Dement Geriatr Cogn Dis Extra.

Abstract

Objective: We aimed to identify biomarkers of Alzheimer's disease (AD) in order to improve diagnostic accuracy at mild stage.

Methods: AD patients aged >50 years were included in the disease group. We evaluated the relationship between potential blood and cerebrospinal fluid inflammatory biomarkers, cognitive status, temporal lobe atrophy and disease severity. Inflammatory biomarkers including interleukin 6 (IL-6), IL-18, fractalkine and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) levels were measured. APOE genotypes were determined.

Results: We enrolled 41 subjects in the disease group and 40 subjects in the normal control group. The majority (88.9%) of subjects in the disease group had mild AD. Elevated levels of plasma IL-6 and decreased levels of plasma TRAIL in the disease group were noted. Plasma levels of IL-6 and TRAIL were significantly correlated with their cerebrospinal fluid levels.

Conclusion: Plasma IL-6 and TRAIL were identified as potential biomarkers of AD at an early stage.

Keywords: Alzheimer's disease; Biomarker; IL-6; Neuroinflammation; TRAIL.

Figures

Fig. 1
Fig. 1
Relationships between cognitive test scores and temporal atrophy index. a, b Positive correlation between CERAD score and rMMSE (a) and between CERAD score and clock drawing test score (b), analyzed by Pearson correlation (both p < 0.0001). c Reduced CERAD score as disease severity increased, analyzed by Kruskal-Wallis test (p < 0 0001). d Negative correlation between temporal atrophy index and CERAD score, analyzed by Pearson correlation (p < 0.01).
Fig. 2
Fig. 2
Plasma levels of IL-6 in the AD and in the normal control group (N). Elevated plasma levels of IL-6 in the AD group compared to the normal control group by unequal variance t test (with Welch's correction) are seen.
Fig. 3
Fig. 3
Plasma levels of TRAIL in the AD and in the normal control group (N). Decreased plasma levels of TRAIL in the AD group compared to the normal control group by unpaired t test are seen.
Fig. 4
Fig. 4
Levels of IL-18 in different disease severities. No significant difference among plasma IL-18 levels of different disease severities was found by Kruskal-Wallis test, although the mean level in the CDR >1 group was reduced compared to the CDR = 0.5 or the CDR = 1 group. n.s. = Not significant.
Fig. 5
Fig. 5
Correlation between CSF and plasma levels of TRAIL (a) and IL-6 (b). Highly correlated plasma levels of TRAIL and IL-6 with each of their CSF levels were found by Pearson correlation.

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References

    1. Knopman DS, et al. Practice parameter: diagnosis of dementia (an evidence-based review). Report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology. 2001;56:1143–1153. - PubMed
    1. Beach TG, Monsell SE, Phillips LE, Kukull W. Accuracy of the clinical diagnosis of Alzheimer disease at National Institute on Aging Alzheimer Disease Centers, 2005-2010. J Neuropathol Exp Neurol. 2012;71:266–273. - PMC - PubMed
    1. Hort J, Bartos A, Pirttila T, Scheltens P. Use of cerebrospinal fluid biomarkers in diagnosis of dementia across Europe. Eur J Neurol. 2010;17:90–96. - PubMed
    1. Keller JN, et al. Evidence of increased oxidative damage in subjects with mild cognitive impairment. Neurology. 2005;64:1152–1156. - PubMed
    1. Krstic D, Knuesel I. Deciphering the mechanism underlying late-onset Alzheimer disease. Nat Rev Neurol. 2012;9:25–34. - PubMed
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