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Published in: Journal of Neuroinflammation 1/2004

Open Access 01-12-2004 | Review

Using animal models to determine the significance of complement activation in Alzheimer's disease

Author: David A Loeffler

Published in: Journal of Neuroinflammation | Issue 1/2004

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Abstract

Complement inflammation is a major inflammatory mechanism whose function is to promote the removal of microorganisms and the processing of immune complexes. Numerous studies have provided evidence for an increase in this process in areas of pathology in the Alzheimer's disease (AD) brain. Because complement activation proteins have been demonstrated in vitro to exert both neuroprotective and neurotoxic effects, the significance of this process in the development and progression of AD is unclear. Studies in animal models of AD, in which brain complement activation can be experimentally altered, should be of value for clarifying this issue. However, surprisingly little is known about complement activation in the transgenic animal models that are popular for studying this disorder. An optimal animal model for studying the significance of complement activation on Alzheimer's – related neuropathology should have complete complement activation associated with senile plaques, neurofibrillary tangles (if present), and dystrophic neurites. Other desirable features include both classical and alternative pathway activation, increased neuronal synthesis of native complement proteins, and evidence for an increase in complement activation prior to the development of extensive pathology. In order to determine the suitability of different animal models for studying the role of complement activation in AD, the extent of complement activation and its association with neuropathology in these models must be understood.
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Metadata
Title
Using animal models to determine the significance of complement activation in Alzheimer's disease
Author
David A Loeffler
Publication date
01-12-2004
Publisher
BioMed Central
Published in
Journal of Neuroinflammation / Issue 1/2004
Electronic ISSN: 1742-2094
DOI
https://doi.org/10.1186/1742-2094-1-18

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