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Infection01:20

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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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The human immune system is a complex network of cells, tissues, and organs that work together to defend the body against bacterial infections. It consists of various immune cells, each playing a specific role in the defense mechanism.
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Related Experiment Video

Updated: Jan 7, 2026

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

Han Noo Ri Lee1, Fiona E Harrison2, Julie A Bastarache2

  • 1Vanderbilt University, Nashville, TN, USA.

Alzheimer'S & Dementia : the Journal of the Alzheimer'S Association
|December 24, 2025
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Summary
This summary is machine-generated.

Aged mice show persistent cognitive deficits after sepsis, not increased brain inflammation. Young mice experienced heightened inflammation but no behavioral changes, suggesting differential inflammatory responses may cause cognitive issues in older adults.

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Area of Science:

  • Neuroscience
  • Immunology
  • Gerontology

Background:

  • Sepsis triggers a significant inflammatory response, often leading to delirium.
  • Delirium in sepsis survivors, especially older adults, predicts Alzheimer's disease and related dementias (ADRD).
  • Mechanisms linking sepsis, delirium, and cognitive decline in aging are poorly understood.

Purpose of the Study:

  • To investigate age-related differences in neuroinflammation and cognitive deficits following polymicrobial sepsis.
  • To test the hypothesis that aged brains exhibit heightened neuroinflammation during sepsis, correlating with persistent cognitive deficits.

Main Methods:

  • Young (3-month) and aged (18-month) wild-type mice were subjected to cecal slurry (CS) to induce sepsis.
  • Sickness severity was monitored, with CS dosage adjusted by age for comparable illness.
  • Cognitive function (nest-building) and neuroinflammation markers were assessed post-sepsis.

Main Results:

  • Aged mice had higher sepsis mortality and persistent nest-building deficits, unlike young mice.
  • Young mice showed heightened systemic inflammation post-sepsis, while aged mice did not exhibit increased neuroinflammation.
  • No significant neuronal damage markers were found in either age group.

Conclusions:

  • Age influences sepsis outcomes, affecting mortality, inflammation, and behavior.
  • Contrary to the hypothesis, aged mice did not show increased neuroinflammation but exhibited persistent cognitive deficits.
  • Differential inflammatory responses to sepsis, not just increased inflammation, may underlie cognitive deficits in aged individuals.