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Inflammatory Mechanisms of Alzheimer’s Disease

Basic Research, Clinical Studies, and Future Directions

  • Chapter
Neuroinflammation

Part of the book series: Contemporary Neuroscience ((CNEURO))

Abstract

Basic research and clinical studies have established that inflammation may play a role in the neurodegeneration that characterizes Alzheimer’s disease (AD). Although inflammation is most likely to arise as a secondary response to more primary events in the development of AD, it is important to recognize that, secondary or not, brain inflammation almost always carries with it the potential to do as much or more damage than the etiology that gave rise to it. For example, the inflammation engendered by a blow to the head is often of greater neurologic consequence than the blow itself. In AD, moreover, there is evidence not only for the classical destructive mechanisms of peripheral inflammation, but also for idiosyncratic interactions of complement, cytokines, acute-phase reactants, and other inflammatory elements with AD pathology. For example, amyloid β peptide (Aβ) has been found to activate complement in an antibody-independent fashion (1, 2),as well as to activate microglia, stimulating them to produce reactive nitrogen intermediates and toxic cytokines, such as TNFα (3) and IL-1 (4). Aβ deposits are present from preclinical to terminal AD. This means that the AD brain harbors pervasive, chronic stimuli that can sustain opsonization, anaphylatoxin generation, complement lysis, cytokine production, and other inflammatory sequelae throughout the disease course. Accumulated over many years, it is difficult to imagine that these mechanisms, and others that they spawn, would not contribute substantially to AD pathogenesis.

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Authors
  1. Joseph Rogers
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  2. W. S. T. Griffin
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  1. Pharmacology, CoCensys, Inc., Irvine, CA, USA

    Paul L. Wood (Director) (Director)

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Rogers, J., Griffin, W.S.T. (1998). Inflammatory Mechanisms of Alzheimer’s Disease. In: Wood, P.L. (eds) Neuroinflammation. Contemporary Neuroscience. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-59259-473-3_6

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  • DOI: https://doi.org/10.1007/978-1-59259-473-3_6

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