Innate Immunity in Alzheimer's Disease
A Model for Local Inflammatory Reactions
- Kinsmen Laboratory of Neurological Research, Department of Psychiatry University of British Columbia, Vancouver, BC V6T 1Z3
- Address correspondence to EGM. E-mail mcgeer{at}interchange.ubc.ca; fax 604-822-7086.
Abstract
Over the past fifteen years, evidence has been accumulating that there is a chronic inflammatory reaction in areas of the brain affected by Alzheimer's disease. Chronic inflammation, which arises in reaction to an underlying pathology, represents a threat in its own right, wherever it may occur, and can in fact surpass primary affronts upon tissues. The brain, however, is particularly vulnerable because neurons are generally irreplaceable. In the case of Alzheimer's disease, inflammatory processes thus have the potential for turning a relatively slowly progressing condition into one characterized by rapid neurodegeneration.
Amyloid plaques (large extracellular deposits) and neurofibrillary tangles (dense intracellular aggregates) are well-known
histological indicators of Alzheimer's disease. Intriguingly, these pathological hallmarks contain all of the major complement
proteins that are normally associated with immune activation. The afflicted brain tissue shown here has been stained with
antibodies specific for complement proteins.
- © American Society for Pharmacology and Experimental Theraputics 2001
