Chronic inflammation appears an important factor in many of the important diseases of aging. Immunohistochemical evidence for chronic inflammation in affected tissue is seen not only in AD, PD, ALS, and multiple sclerosis but also in other conditions such as atherosclerosis, heart disease, and macular degeneration (Bok, 2005; Kuehn, 2005). Finch (2005), for example, has recently reviewed the "remarkable convergence of inflammatory mechanisms in the etiology of cardiovascular disease and Alzheimer disease." The more than 20 epidemiological studies indicating that chronic use of nonsteroidal antiinflammatory drugs (NSAIDs) greatly reduces the risk of AD testifies to the importance of the inflammatory reaction (McGeer & McGeer, 2004a). And recently single epidemiological studies have been published indicating that such use of NSAIDs also reduces the risk of PD (Chen et al., 2003) and macular degeneration (McGeer & Sibley, 2005). Moreover, forms of various inflammatory mediators which favor their production have been reported to increase the risk of AD (McGeer & McGeer, 2004a), PD (McGeer & McGeer, 2004b), and macular degeneration (Scholl, Weber, Nothen, Wienker, & Holz, 2005). Research on methods of controlling the inflammatory activation of microglia, while retaining their beneficial functions, and reducing formation of the MAC of complement would therefore seem to deserve high priority.
Acknowledgment. Our research has been supported by grants from the Jack Brown and Family A.D. Research Fund, the Pacific Parkinson Foundation, and the Alzheimer Society of Canada-CIHR-AstraZeneca Co., as well as donations from the estate of George Hodgson, The Friends of UBC and individual British Columbians.
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