Decline of immune responsiveness: A pathogenetic factor in Alzheimer's disease?
Decline of immune responsiveness: A pathogenetic factor in Alzheimer's disease?
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DOI:
10.1016/j.jpsychires.2004.12.005
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发表时间:
2005-09-01
影响因子:
4.8
通讯作者:
Schott, K
中科院分区:
文献类型:
--
作者:
Richartz, E;Stransky, E;Schott, K
The involvement of immunological alterations in the pathogenesis of Alzheimer's disease (AD) is widely discussed. Hitherto, findings on systemic immunological alterations are inconsistent. We measured the concentrations of the pro-inflammatory cytokines IL-1 beta, IL-2, IL-6, and TNF-alpha, and of the soluble receptors sIL-2r, sIL-6r, and sTNF-alpha r, in cerebrospinal fluid (CSF) and serum of 20 Alzheimer patients and 21 controls. Moreover, we studied levels of the pro-inflammatory IL-6, Il-12, IFN-gamma, and TNF-alpha, and of the anti-inflammatory IL-5 and IL-13 in stimulated blood cell cultures from 27 AD patients and 25 controls. The levels in CSF and serum were diminished in AD or under detection limit. In mitogen-stimulated blood cultures we found a significant decrease of pro- and anti-inflammatory cytokines in the AD group. Our data suggest a general decline of immune responsiveness in AD. Based on the recent research, an impaired immune response may be considered as a pathogenetically relevant factor in AD. With respect to the putative role of ageing in AD, we assume a premature immunosenescence contributing to the Alzheimer's pathology. (c) 2005 Elsevier Ltd. All rights reserved.