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Inflammation and Alzheimer's disease pathogenesis

J Rogers1, S Webster, L F Lue

  • 1Sun Health Research Institute, Sun City, AZ 85372, USA.

Neurobiology of Aging
|September 1, 1996
PubMed
Summary

Inflammation plays a key role in Alzheimer's disease (AD) pathogenesis, potentially causing neurodegeneration and benefiting from anti-inflammatory treatments. This review challenges misconceptions about inflammation's role in AD progression.

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Area of Science:

  • Neuroscience
  • Immunology
  • Pathology

Background:

  • Misconceptions regarding inflammation's role in Alzheimer's disease (AD) pathogenesis hinder understanding.
  • Inflammation is often viewed as secondary to neurodegeneration or merely clearing debris.

Purpose of the Study:

  • To reassess the role of inflammatory mediators in Alzheimer's disease (AD) pathogenesis.
  • To challenge the notion that neurodegenerative mechanisms must be primary to be significant.
  • To investigate if inflammation is a necessary or sufficient cause of AD neurodegeneration.

Main Methods:

  • Review of existing literature on inflammatory molecules and mechanisms in the AD brain.
  • Analysis of retrospective and direct clinical trials of anti-inflammatory medications in AD patients.

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Main Results:

  • Inflammatory molecules and mechanisms are significantly elevated in the AD brain.
  • Evidence suggests inflammation may be a necessary component of AD pathogenesis.
  • Inflammation may be sufficient to cause neurodegeneration in AD.
  • Clinical trials indicate anti-inflammatory drugs may slow AD progression or delay onset.

Conclusions:

  • Inflammation is a critical factor in Alzheimer's disease pathogenesis, not just a response to it.
  • Targeting inflammatory pathways with anti-inflammatory medications shows therapeutic potential for AD.