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When a pathogen enters the body and reproduces, it can cause an infection, damage body cells, and cause illness symptoms that eventually lead to disease. Therefore, its prevention requires breaking the chain of infection.
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Basic Science and Pathogenesis.

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Systemic bacterial infection in Alzheimer

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Area of Science:

  • Neuroscience
  • Immunology
  • Pathology

Background:

  • Alzheimer's Disease (AD) pathology involves amyloid-beta and tau tangles, with immune system activation playing a critical role.
  • Systemic infections can exacerbate cognitive decline in AD patients, potentially via cerebrovascular and neuroinflammatory pathways.
  • Traditional models using lipopolysaccharide (LPS) do not fully replicate chronic low-grade inflammation seen in real bacterial infections.

Purpose of the Study:

  • To investigate the inflammatory and vascular consequences of a live bacterial infection (Salmonella Typhimurium) in Alzheimer's Disease (APP/PS1) mice.
  • To compare these effects against wild-type (WT) mice to understand disease-specific responses.

Main Methods:

  • APP/PS1 and WT mice were infected with live attenuated Salmonella Typhimurium or saline control.
  • Liver and brain tissues were collected at 7 and 28 days post-infection.
  • Immunofluorescence was used to analyze systemic inflammation, cerebrovascular dysfunction, and neuroinflammation.

Main Results:

  • Salmonella Typhimurium infection induced fibrinogen deposition and inflammatory lesions in the liver.
  • Cerebrovascular activation (increased VCAM, ICAM) and fibrinogen/IgG extravasation into the brain occurred by day 7.
  • APP/PS1 mice exhibited an exaggerated microglial response (MHC-II, FcγRI) compared to WT mice.

Conclusions:

  • Systemic bacterial infection leads to an exaggerated microglial neuroinflammatory response in APP/PS1 mice.
  • Cerebrovascular dysfunction and fibrin-mediated microglial activation likely contribute to this heightened neuroinflammation.
  • This model provides insights into how systemic infections impact AD progression.