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Article type: Research Article
Authors: Busse, Stefana; * | Steiner, Johanna; b | Alter, Julianea | Dobrowolny, Henrika | Mawrin, Christianc | Bogerts, Bernharda; b | Hartig, Rolandd | Busse, Mandye
Affiliations: [a] Department of Psychiatry, University of Magdeburg, Magdeburg, Germany | [b] Center for Behavioral Brain Sciences, Magdeburg, Germany | [c] Department of Neuropathology, University of Magdeburg, Magdeburg, Germany | [d] Institute of Immunology, University of Magdeburg, Magdeburg, Germany | [e] Department of Pediatric Pulmonology, Allergology & Neonatology, Medical University of Hannover, Hannover, Germany
Correspondence: [*] Correspondence to: Stefan Busse, MD, Department ofPsychiatry, University of Magdeburg, Leipziger Str. 44, D-39120 Magdeburg, Germany. Tel.: +49 391 67 14233; Fax: +49 391 67 15035; [email protected]
Abstract: Although monocytes and macrophages could serve as new therapeutic targets for treatment of Alzheimer’s disease (AD) and aging of the human innate immune system, its role in the pathogenesis of neurodegenerative disorders such as AD are only poorly understood. We have addressed this here by determining the number of CD14+ monocytes and the frequency of HLA-DR-, CD80-, and CD86-expression in peripheral blood from healthy volunteers aged 20–79 years, and in AD patients at diagnosis and after 12, 30, and 52 weeks of rivastigmine treatment. While the number of CD14+ monocytes remained constant, the expression of HLA-DR, CD80, and CD86 by monocytes increased with age. However, no differences were identified by comparing AD patients with age-matched healthy controls or following treatment of AD patients with rivastigmine. These results indicate that changes in the expression of HLA-DR, CD80, and CD86 are caused by immunosenescence rather than by AD pathology or treatment of AD patients with rivastigmine.
Keywords: Alzheimer’s disease, monocytes, CD80, CD86, HLA-DR
DOI: 10.3233/JAD-150217
Journal: Journal of Alzheimer's Disease, vol. 47, no. 1, pp. 177-184, 2015
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