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J Neuropsychiatry Clin Neurosci 19:318-325, August 2007
doi: 10.1176/appi.neuropsych.19.3.318
© 2007 American Neuropsychiatric Association
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Circulating Interleukin-15 in Dementia Disorders

Michael Rentzos, M.D., George P. Paraskevas, M.D., Elisabeth Kapaki, M.D., Chryssoula Nikolaou, M.D., Margarita Zoga, M.D., Anthousa Tsoutsou, M.D., Antonis Rombos, M.D. and Demetrios Vassilopoulos, Ph.D.

Received May 9, 2006; revised August 5, 2006; accepted August 21, 2006. Drs. Rentzos, Paraskevas, Kapaki, Rombos, and Vassilopoulos are affiliated with the Department of Neurology, Aeginition Hospital, Athens National University, School of Medicine, Athens, Greece. Drs. Nikolau, Zoga, and Tsoutsou are affiliated with the Department of Immunology, Aeginition Hospital, Athens National University, School of Medicine, Athens, Greece. Address correspondence to Dr. Rentzos, Aeginition Hospital, Athens National University, School of Medicine, 72–74 Vas. Sophias Avenue, Athens 11528, Greece; mrentzos{at}med.uoa.gr (e-mail).

The objective of this study was to assess the role of interleukin-15 (IL-15) as a potential marker of immune reactions in patients with Alzheimer’s disease and vascular dementia. The authors measured by immunoassay serum IL-15 levels in 20 patients with Alzheimer’s disease and 15 patients with vascular dementia and compared them with serum IL-15 levels in 15 healthy subjects. The authors also studied the effect of treatment with acetylcholinesterase inhibitors (AChEI) on serum IL-15 levels. Patients with Alzheimer’s disease were found to have significantly lower serum IL-15 levels compared with healthy subjects and patients with vascular dementia. Healthy subjects and patients with vascular dementia did not differ between each other. Age, sex, disease duration, and Mini-Mental State Examination score did not affect IL-15 levels in any of the groups. Treatment with AChEI had no influence on IL-15 concentrations. The findings suggest that IL-15 is not implicated in the pathogenetic mechanisms of Alzheimer’s disease and vascular dementia. An immune hyporesponsiveness at some point during disease development may be responsible for the lower levels of IL-15 and other cytokines in Alzheimer’s disease patients.







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