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Peripheral Expression of IL-6, TNF-α and TGF-β1 in Alzheimer’s Disease Patients
Gamze Güven1, Pınar Köseoğlu1, Ebba Lohmann2, Bedia Samancı3, Erdi Şahin3, Başar Bilgiç3, Haşmet Ayhan Hanağası3, Hakan Gürvit3, Nihan Erginel-Ünaltuna11İstanbul University, Aziz Sancar Institute of Experimental Medicine, Department of Genetics, İstanbul, Turkey2Department of Neurodegenerative Diseases, Hertie Institute for Clinical Brain Research, University of Tübingen, Germany; Dzne, German Center for Neurodegenerative Diseases, Tübingen, Germany
3Behavioural Neurology and Movement Disorders Unit, Department of Neurology, İstanbul Faculty of Medicine, İstanbul University, İstanbul, Turkey
Objective: Neuroinflammation is involved in the pathology of Alzheimer’s disease (AD). Peripheral levels of various inflammatory cytokines are altered during AD pathogenesis. This study aimed to examine the role of peripheral inflammation in AD pathogenesis by measuring serum levels and gene expression of specific inflammatory cytokines in AD patients. Therefore, we analyzed serum interleukin-6 (IL-6) and transforming growth factor-beta 1 (TGF-β1) levels and mRNA expressions of IL-6 and tumor necrosis factor-alpha (TNF-α) in peripheral blood mononuclear cells of AD patients and controls.
Materials and Methods: We quantitatively assessed serum IL-6 and TGF-β1 levels in 25 AD patients and 33 age-matched controls using enzymelinked immunosorbent assay. In addition, we evaluated the mRNA expressions of IL-6 and TNF-α in peripheral blood mononuclear cells from 31 AD patients and their respective controls (n=30) via quantitative real-time polymerase chain reaction.
Results: AD patients tended to have higher serum IL-6 and TGF-β1 levels compared to the controls, but the difference was not statistically significant. IL-6 and TNF-α mRNA expression was significantly downregulated in AD patients compared to the controls (p=0.000 and p=0.004; respectively). Serum IL-6 and TGF-β1 levels were negatively correlated with age in AD patients (p=0.025, r=-0.467 and p=0.035, r=-0.431; respectively).
Conclusion: The outcomes of this study suggest a disruption in the peripheral immune response in individuals with AD. The observed decreased expression of cytokine genes in peripheral leukocytes may indicate a contributory mechanism through which peripheral cytokines influence AD pathogenesis.
Manuscript Language: English
