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      Inflammation and Alzheimer's disease.

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          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.

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          Author and article information

          Journal
          Neurobiol Aging
          Neurobiology of aging
          Elsevier BV
          0197-4580
          0197-4580
          June 20 2000
          : 21
          : 3
          Affiliations
          [1 ] Sun Health Research Institute, 10515 West Santa Fe Drive, P.O. Box 1278, 85372, Sun City, AZ, USA.
          Article
          S019745800000124X NIHMS542954
          10.1016/s0197-4580(00)00124-x
          3887148
          10858586
          69a4786a-d6cd-4c63-9c35-babdfb771edf

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