Organization of Inflammatory Processes in Alzheimer’s Disease

Summary

Basic research and clinical studies have established inflammation as one of several important pathogenic mechanisms in Alzheimer’s disease (AD). The sources of inflammation appear to be aggregated amyloid β peptide deposits, neurofibrillary tangles, and neurodegeneration itself. Organization of the inflammatory mediators and processes that have been uncovered in AD is likely to follow patterns similar to those observed in the periphery.

Over the last decade a virtual textbook of inflammatory mediators has been observed in the Alzheimer’s disease (AD) brain. They are almost universally increased in expression in comparision to brain samples from the normal elderly (ND), and the are most often concentrated in regions of the brain that exhibit selective AD vulnerability (reviewed in Rogers and Griffin 1997; Rogers and O’Barr 1996; Rogers et al. 1996).

In broad scope how these inflammatory molecules and processes are organized should not be a great mystery. We have nearly a century of information from peripheral immunology that links, for example, complement to cytokines and cytokines back to complement. By judicious review of the same textbooks that we used as undergraduate and graduate students, we should therefore be able to arrive at a reasonable approximation of the way inflamation works in the AD brain.