Evidence that neuroinflammation exacerbates the pathology in Alzheimer’s disease (AD) has been accumulated from three independent fields of research: neuropathology demonstrating activated glial cells, epidemiology showing sparing of AD in individuals consuming anti-inflammatory drugs, and AD transgenic animal studies showing protection from COX-1-inhibiting drugs. Similar findings have now been established for Parkinson’s disease. Inflammation accompanies the lesions; epidemiological studies show a sparing effect of NSAIDs; and anti-inflammatory agents are protective in animal models of the disease. Inflammation is not believed to be the triggering event in these conditions, but nevertheless is capable of chronically exacerbating the pathology. It is characterized by the generation of a spectrum of inflammatory mediators produced locally by resident cells. Such local production indicates engagement of the innate immune system. Similar phenomena are now being observed in degenerative peripheral conditions such as diabetes type 2. A distinction needs to be made between these autotoxic disorders and classical autoimmune disorders, which involve participation of the adaptive immune system. The adaptive immune system is more powerful, resulting in a range of autoimmune diseases that are more severe and strike at a younger age. Autotoxic diseases, being milder, occur in the aging population but overall are more prevalent than autoimmune diseases. Both immune systems use local phagocytes such as microglia to be the effecter cells so that methods to reduce the toxic effects of their overstimulation should be beneficial in a broad spectrum of human diseases.
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