INFLAMMATION IS a routine consequence of general body tissue injury in higher organisms. Classic inflammation, with infiltration of lymphocytes and/or macrophages also occurs in the central nervous system, notably following brain injury from stroke or trauma, as well as in various "autoimmune" or infectious cerebral disorders. However, brains of patients with degenerative diseases of the central nervous system, such as Alzheimer, Pick, Parkinson, or Huntington diseases, do not generally show classic signs of inflammation. Nevertheless, a large body of work, notably pioneered by E. G. McGeer, PhD, P. L. McGeer, MD, PhD, J. Rogers, PhD, and colleagues, has shown that despite the absence of notable lympho-infiltrative processes, there is, indeed, neuropathological evidence for immune activation in the most common neurodegenerative disease in aging humans, namely, Alzheimer disease (AD).1-4 Abnormal deposition of complement components, acute-phase reactants, and various cytokines, up-regulation of cyclooxygenase-2, and microgliosis with expression of class II major histocompatibility complex antigens (HLA-DR) are among the features that have been noted in this chronic disease. Many of these changes have also been observed in mouse transgenic models of AD. However, the role of these brain changes, characteristic of immune activation, in the pathogenesis of the disease is uncertain.
Honig LS. Inflammation in Neurodegenerative Disease: Good, Bad, or Irrelevant? Arch Neurol. 2000;57(6):786–788. doi:10.1001/archneur.57.6.786
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