Twenty years ago it was recognized that inflammatory mechanisms play a pathogenic role in multiple sclerosis, but for other disorders the brain was generally considered to be “immunologically privileged.” This view began to change with the discovery that microglia in the Alzheimer’s disease (AD) cortex were activated (e.g., immunoreactive for the major histocompatibility complex),1,2 similar to peripheral macrophages at sites of inflammation. We now know that cytokines, complement, reactive oxygen and nitrogen species, and other markers of inflammation are highly upregulated in a wide range of neurodegenerative disorders, particularly AD.3 This should not be surprising because, by definition, tissue damage occurs in neurodegenerative disorders, and inflammation is a normal response to tissue damage wherever it occurs in the body. In addition, the chronic presence of highly inert, highly insoluble deposits is another classic inflammatory stimulus, and such deposits are present by the millions in the AD brain as amyloid β peptide (Aβ) plaques and neurofibrillary tangles.