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Basic Science and Pathogenesis.

Quan Vo1, Dina Nacionales1, Kristi Biswas1

  • 1University of Florida, Gainesville, FL, USA.

Alzheimer'S & Dementia : the Journal of the Alzheimer'S Association
|December 25, 2025
PubMed
Summary
This summary is machine-generated.

Systemic inflammation did not accelerate tau pathology in a mouse model of Alzheimer's disease (AD). However, sepsis impacted lifespan and brain tau levels differently in male and female mice.

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Area of Science:

  • Neuroscience
  • Immunology
  • Pathology

Background:

  • Inflammation is a key factor in Alzheimer's disease (AD) neurodegeneration.
  • Previous studies show intracerebral inflammation affects tau pathology in AD models.
  • The impact of chronic peripheral inflammation on brain tau remains unclear.

Purpose of the Study:

  • To investigate if chronic peripheral inflammation alters brain-resident tau protein.
  • To examine the effects of sepsis on tau pathology and immune responses in PS19 mice.

Main Methods:

  • Induced intra-abdominal sepsis and chronic stress in PS19 mice (transgenic for human P301S mutant tau).
  • Collected brain and spleen tissues for immunohistochemistry and flow cytometry.
  • Assessed phosphorylated tau (AT8) and immune cell alterations in prodromal and survival cohorts.

Main Results:

  • Systemic inflammation did not accelerate AT8-positive tau pathology in either sex.
  • Sepsis altered immune cell distribution, including reduced CD8+ T-cells in females and increased myeloid-derived suppressor cells in both sexes.
  • Sex-specific differences observed in lifespan and regional AT8-tau burden, with male septic mice showing lower hippocampal tau.

Conclusions:

  • Systemic inflammation can influence lifespan and regional tau burden in an Alzheimer's disease mouse model in a sex-dependent manner.
  • Further research is needed to elucidate the mechanistic links between systemic inflammation and AD-type tau pathology.