Akiyama, Haruhiko; Barger, Steven; Barnum, Scott; Bradt, Bonnie; Bauer, Joachim; Cole, Greg M.; Cooper, Neil
R.; Eikelenboom, Piet; Emmerling, Mark; Fiebich, Berndt L.; Finch, Caleb E.; Frautschy, Sally; Griffin, W.S.T.;
Hampel, Harald; Hull, Michael; Landreth, Gary; Lue, Lih-Fen; Mrak, Robert; Mackenzie, Ian R.; McGeer, Patrick
L.; O'Banion, M. Kerry; Pachter, Joel; Pasinetti, Guilio; Plata-Salaman, Carlos; Rogers, Joseph; Rydel, Russell;
Shen, Yong; Streit, Wolfgang; Strohmeyer, Ronald; Tooyoma, Ikuo; Van Muiswinkel, Freek L.; Veerhuis, Robert;
Walker, Douglas; Webster, Scott; Wegrzyniak, Beatrice; Wenk, Gary; Wyss-Coray, Tony.
Inflammation and Alzheimer's disease,
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 b 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.
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