Inflammation and Alzheimer's disease - PubMed (original) (raw)

Review

. 2000 May-Jun;21(3):383-421.

doi: 10.1016/s0197-4580(00)00124-x.

S Barger, S Barnum, B Bradt, J Bauer, G M Cole, N R Cooper, P Eikelenboom, M Emmerling, B L Fiebich, C E Finch, S Frautschy, W S Griffin, H Hampel, M Hull, G Landreth, L Lue, R Mrak, I R Mackenzie, P L McGeer, M K O'Banion, J Pachter, G Pasinetti, C Plata-Salaman, J Rogers, R Rydel, Y Shen, W Streit, R Strohmeyer, I Tooyoma, F L Van Muiswinkel, R Veerhuis, D Walker, S Webster, B Wegrzyniak, G Wenk, T Wyss-Coray

Affiliations

Review

Inflammation and Alzheimer's disease

H Akiyama et al. Neurobiol Aging. 2000 May-Jun.

Abstract

Inflammation clearly occurs in pathologically vulnerable regions of the Alzheimer's disease (AD) brain, and it does so with the full complexity of local peripheral inflammatory responses. In the periphery, degenerating tissue and the deposition of highly insoluble abnormal materials are classical stimulants of inflammation. Likewise, in the AD brain damaged neurons and neurites and highly insoluble amyloid beta peptide deposits and neurofibrillary tangles provide obvious stimuli for inflammation. Because these stimuli are discrete, microlocalized, and present from early preclinical to terminal stages of AD, local upregulation of complement, cytokines, acute phase reactants, and other inflammatory mediators is also discrete, microlocalized, and chronic. Cumulated over many years, direct and bystander damage from AD inflammatory mechanisms is likely to significantly exacerbate the very pathogenic processes that gave rise to it. Thus, animal models and clinical studies, although still in their infancy, strongly suggest that AD inflammation significantly contributes to AD pathogenesis. By better understanding AD inflammatory and immunoregulatory processes, it should be possible to develop anti-inflammatory approaches that may not cure AD but will likely help slow the progression or delay the onset of this devastating disorder.

PubMed Disclaimer

Similar articles

Cited by

References

    1. . The Canadian Study of Health and Aging: risk factors for Alzheimer’s disease in Canada. Neurology. 1994;44:2073–80. - PubMed
    1. Abraham CR, Selkoe DJ, Potter H. Immunochemical identification of the serine protease inhibitor alpha 1-antichymotrypsin in the brain amyloid deposits of Alzheimer’s disease. Cell. 1988;52:487–501. - PubMed
    1. Adams DO, Hamilton TA. The Macrophage. Oxford: IRL; 1992. Molecular basis of macrophage activation.
    1. Afagh A, Cummings BJ, Cribbs DH, Cotman CW, Tenner AJ. Localization and cell association of C1q in Alzheimer’s disease brain. Exp Neurol. 1996;138:22–32. - PubMed
    1. Aguado F, Ballabriga J, Pozas E, Ferrer I. TrkA immunoreactivity in reactive astrocytes in human neurodegenerative diseases and colchicine-treated rats. Acta Neuropathol (Berlin) 1998;96:495–501. - PubMed

Publication types

MeSH terms

LinkOut - more resources