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Mouse Footpad Inoculation Model to Study Viral-Induced Neuroinflammatory Responses
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Basic Science and Pathogenesis.

Arash Salardini1,2,3, Arsalan Hashemi-Aghdam4, Ryan S O'Dell5,6

  • 1University of Texas Health Science Center, San Antonio, TX, USA.

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

Individuals with Alzheimer's disease (AD) show reduced microglial activation following immune challenges, challenging existing neuroinflammation models. This suggests therapies should focus on restoring microglial function rather than broad suppression.

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Area of Science:

  • Neuroscience
  • Immunology
  • Radiochemistry

Background:

  • Alzheimer's disease (AD) is marked by chronic neuroinflammation and altered microglial function.
  • Limited efficacy of current anti-inflammatory therapies may stem from impaired microglial reactivity.
  • Experimental endotoxemia using lipopolysaccharide (LPS) offers a model to study in vivo microglial responses.

Purpose of the Study:

  • To investigate if AD is associated with blunted microglial activation in response to LPS.
  • To utilize positron emission tomography (PET) with the translocator protein (TSPO) tracer [11C]PBR28 to quantify microglial response.
  • To assess microglial activation reserve using the Microglial Activation Reserve Index (MARI).

Main Methods:

  • 12 participants (6 healthy controls [HC], 6 with mild cognitive impairment [MCI] or AD) underwent [11C]PBR28 PET scans.
  • Scans were performed before and 3 hours after LPS administration.
  • MARI was calculated as the percentage change in regional volume of distribution (VT) post-LPS; cognitive and safety data were collected.

Main Results:

  • The MCI/AD group showed a trend towards blunted microglial response to LPS compared to HC (p=0.064).
  • Robust regression, adjusting for covariates, revealed a significant association between diagnostic status and MARI (p=0.041).
  • Model stability was limited by sample size; no significant adverse effects were observed.

Conclusions:

  • Findings suggest paradoxical impairment in microglial reactivity to immune challenges in AD.
  • This challenges current models of neuroimmune dysfunction in AD.
  • Therapeutic strategies should consider restoring microglial function over broad anti-inflammatory approaches.