When the infectious environment meets the AD brain

Tal Ganz, Nina Fainstein, Tamir Ben-Hur*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

13 Scopus citations

Abstract

Background: The Amyloid theory of Alzheimer’s disease (AD) suggests that the deposition of Amyloid β (Aβ) in the brain triggers a chain of events, involving the deposition of phosphorylated Tau and other misfolded proteins, leading to neurodegeneration via neuroinflammation, oxidative stress, and neurovascular factors. The infectious theory linked various infectious agents with the development of AD, raising the possibility that they serve as etiological causes of the disease. Are these theories mutually exclusive, or do they coincide? Main body: In this review, we will discuss how the two theories converge. We present a model by which (1) the systemic infectious burden accelerates the development of AD brain pathology via bacterial Amyloids and other pathogen-associated molecular patterns (PAMPs), and (2) the developing AD brain pathology increases its susceptibility to the neurotoxicity of infectious agents -derived PAMPs, which drive neurodegeneration via activated microglia. Conclusions: The reciprocal effects of amyloid deposition and systemic infectious burden may lead to a vicious cycle fueling Alzheimer’s disease pathogenesis.

Original languageAmerican English
Article number53
JournalMolecular Neurodegeneration
Volume17
Issue number1
DOIs
StatePublished - Dec 2022

Bibliographical note

Publisher Copyright:
© 2022, The Author(s).

Keywords

  • Alzheimer’s disease
  • Amyloid-β
  • Infection
  • Lipopolysaccharides
  • Microglia
  • Neurodegeneration
  • Neuroinflammation
  • Pathogen associated molecular patterns

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