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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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Updated: Jan 7, 2026

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

Fernanda G Q Barros-Aragão1, Luis E Santos1, Talita Pinto2

  • 1D'Or Institute for Research and Education, Rio de Janeiro, RJ, Brazil.

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

COVID-19 neurological patients show elevated Tau protein, similar to Alzheimer's disease (AD) patients, linked to inflammation. Persistent inflammation and cognitive issues post-COVID-19 may increase future AD risk.

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Area of Science:

  • Neuroscience
  • Immunology
  • Infectious Diseases

Background:

  • COVID-19 can cause neurological symptoms and cognitive decline, with Alzheimer's disease (AD) increasing COVID-19 severity.
  • Inflammation is implicated in both COVID-19 and AD, suggesting a potential molecular link.
  • It remains unclear if COVID-19 patients with neurological issues exhibit AD-related molecular changes.

Purpose of the Study:

  • To investigate molecular alterations related to Alzheimer's disease (AD) pathology in COVID-19 patients with neurological symptoms.
  • To identify potential molecular links between COVID-19 and AD for improved patient follow-up and prevention strategies.

Main Methods:

  • Retrospective analysis of cerebrospinal fluid (CSF) biomarkers (amyloid-beta, Tau) in controls, mild cognitive impairment, AD, and COVID-19 patients with neurological symptoms.
  • Correlation of CSF biomarkers with inflammation markers (IL6, SII).
  • Prospective evaluation of plasma biomarkers (amyloid-beta, Tau) and cognitive outcomes in COVID-19 survivors up to one year post-infection.

Main Results:

  • COVID-19 patients with neurological symptoms showed elevated CSF Tau at hospitalization, similar to AD patients.
  • No significant changes in CSF amyloid-beta or pTau-181 levels were detected in COVID-19 patients.
  • CSF biomarkers and pro-inflammatory cytokines correlated with systemic inflammation (SII).
  • Plasma Tau/amyloid-beta ratio increased in COVID-19 survivors with cognitive deficits one year post-infection.
  • Longitudinal plasma Tau changes were influenced by disease severity, inflammation, and cognitive deficits.

Conclusions:

  • Inflammation is a key factor in acute and persistent AD-related molecular changes observed in COVID-19 patients.
  • COVID-19 survivors with ongoing inflammation or cognitive symptoms require careful monitoring for potential future AD risk.