The classical view of the brain as an immunologically privileged site primarily due to its effective selectivity and the relative impermeability of the blood-brain barrier has made it difficult to consider the notion that inflammatory processes, also classically considered to be a domain of the circulatory system, occur in the brain. But the early findings by the McGeer and Rogers groups, starting as early as 1987, on the expression of immune system antigens (16), the presence of reactive microglia (17), and the activation of the classical compliment pathway in Alzheimer's disease (AD) brain (18) strongly implicated neuroinflammatory processes. In addition, their early demonstrations that rheumatoid patients taking antiinflammatory drugs had delayed appearance of AD symptoms (19) also strongly suggested the importance of neuroinflammatory events in the dementia associated with the disease. The early demonstrations that proinflammatory cy-tokines were shown to be elevated in neurodegenerative conditions (20-23) and that activated microglia cells produce superoxide (23,24) thus also provided a solid foundation for the rationale. Rogers and O'Barr (25) and Floyd (26) recently reviewed the data and ideas of neuroinflammation.
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