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Infectious etiology and amyloidosis in Alzheimer's disease: The puzzle continues

Rakez Kayed1

  • 1Mitchell Center for Neurodegenerative Diseases, Departments of Neurology, Neuroscience and Cell Biology, University of Texas Medical Branch, Galveston, Texas, USA.

The Journal of Biological Chemistry
|July 4, 2021
PubMed

Insights

This study investigated if beta amyloid protects against herpes simplex virus type 1 infection in Alzheimer's disease models. Results showed no protective effect, not confirming nor disproving the infection hypothesis for Alzheimer's disease.

Area of Science:

  • Neuroscience
  • Infectious Diseases
  • Alzheimer's Disease Research

Background:

  • The role of infectious agents in late-onset Alzheimer's disease (AD) is a subject of ongoing debate.
  • Previous research has explored potential links between microbial pathogens and AD pathogenesis.

Purpose of the Study:

  • To investigate the potential antiviral properties of human beta amyloid (Aβ) against herpes simplex virus type 1 (HSV-1) infection.
  • To assess the impact of abundant Aβ expression on susceptibility to HSV-1 in a mouse model of Alzheimer's disease.

Main Methods:

  • Utilized 5XFAD transgenic mice with abundant human beta amyloid (Aβ) expression in the brain.
  • Infected mice with acute herpes simplex virus type 1 (HSV-1).
  • Compared infection outcomes in 5XFAD mice with control mice.

Main Results:

  • Abundant expression of human beta amyloid (Aβ) in the mouse brain did not confer protection against acute herpes simplex virus type 1 (HSV-1) infection.
  • No significant difference in protection was observed between 5XFAD animals and control mice regarding HSV-1 infection.

Conclusions:

  • The study does not confirm antiviral actions of beta amyloid (Aβ) against herpes simplex virus type 1 (HSV-1).
  • Findings neither support nor disprove the hypothesis that microbial pathogen infection is a primary cause of Alzheimer's disease.

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