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Pattern of interleukin-6 receptor complex immunoreactivity between cortical regions of rapid autopsy normal and Alzheimer’s disease brain

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Abstract

Involvement of the interleukin–6 receptor complex (IL–6RC) in neuroregulatory and immunological processes of the brain and particularly in Alzheimer’s disease (AD) has been hypothesized. The functionally active IL–6RC consists of the cytokine IL–6, which acts through the ligand binding IL–6R and the signal transducing gp130. Using a new immunocytochemical protocol on rapid autopsy cryostat brain sections we studied the expression of the IL–6RC in Braak IV–V staged AD patients compared to normal age–matched controls (HC) across five different cortical regions. Inter–rater reliability of the method was high. The “baseline” expression in normal human brain was determined for IL–6,IL–6R and gp130 in all cortical regions. In normal tissue IL–6 expression was lower in parietal cortex. Higher IL–6R expression was shown in frontal, occipital and parietal cortex, lower expression in temporal cortex and cerebellum. In AD IL–6 expression levels were generally increased in parietal cortex and decreased in occipital cortex compared to controls. IL–6R expression levels were strongly increased in AD frontal and occipital cortex and decreased in temporal cortex and cerebellum. Our findings indicate an altered cortical immunoreactivity pattern of the functional IL–6RC in AD supporting the hypothesis of a disease–related role of IL–6 in AD pathophysiology.

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Preliminary parts of this work were presented in abstract form at the 28th Annual Meeting of the Society of Neuroscience, Los Angeles, CA, 1998, at the 29th Annual Meeting of the Society of Neuroscience, Miami, FL, 1999, at the Neuroinflammation Conference, Washington, DC, 2000 and at the 30th Annual Meeting of the Society of Neuroscience, New Orleans, LA, 2000.

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Hampel, H., Haslinger, A., Scheloske, M. et al. Pattern of interleukin-6 receptor complex immunoreactivity between cortical regions of rapid autopsy normal and Alzheimer’s disease brain. Eur Arch Psychiatry Clin Neurosci 255, 269–278 (2005). https://doi.org/10.1007/s00406-004-0558-2

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