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Basic Science and Pathogenesis.

Autumn Meek1, Matthew P Neal1, Donald F Weaver2

  • 1Krembil Research Institute, Toronto, ON, Canada.

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Alzheimer's disease (AD) is proposed as a persistent neuroinflammatory disorder driven by innate immunity. Amyloid-beta (Aβ) acts as an immunopeptide, initiating a self-directed attack on neurons, leading to chronic inflammation.

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Area of Science:

  • Neuroscience
  • Immunology
  • Molecular Biology

Background:

  • Alzheimer's disease (AD) pathogenesis involves multiple proposed mechanisms, including proteopathy, immunopathy, and oxidative stress.
  • A unified model is needed to reconcile divergent theories and advance towards a cure.
  • Characterizing AD as a persistent neuroinflammatory disorder mediated by innate immunity offers a comprehensive framework.

Purpose of the Study:

  • To develop a unifying molecular pathogenesis model for Alzheimer's disease (AD).
  • To integrate various proposed AD mechanisms into a single, comprehensive explanation.
  • To investigate the role of innate immunity in AD pathogenesis.

Main Methods:

  • Performed in silico, in vitro, and in vivo studies.
  • Evaluated Aβ/tau oligomerization, Aβ-mediated membrane rupture, cytokine release, mitochondrial damage, synaptotoxicity, and reactive oxygen species generation.
  • Systematically probed for unifying mechanistic commonalities.

Main Results:

  • Amyloid-beta (Aβ) functions as an antimicrobial and immunomodulatory peptide within the innate immune system.
  • Aβ triggers an innate immunity cascade, misdirecting attacks on neurons due to surface similarities with bacteria.
  • Aβ binding to GM1 on neurons and glial cells initiates neuroinflammation and mitochondrial damage, leading to persistent innate immunity activation.

Conclusions:

  • A novel, unifying model posits Alzheimer's disease as a disorder of persistent innate immunity activation.
  • This model integrates proteopathy, immunopathy, and other mechanisms under the umbrella of innate immune dysregulation.
  • The proposed model provides a comprehensive explanation for AD pathogenesis.