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Updated: Jan 31, 2026

Purification and Aggregation of the Amyloid Precursor Protein Intracellular Domain
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Microglia and amyloid precursor protein coordinate control of transient Candida cerebritis with memory deficits

Yifan Wu1,2, Shuqi Du3, Jennifer L Johnson4,5,6

  • 1Departments of Pathology and Immunology, Baylor College of Medicine, One Baylor Plaza, Houston, TX, 77030, USA.

Nature Communications
|January 6, 2019
PubMed

Insights

This study reveals that Candida albicans bloodstream infections cause brain inflammation and mild memory loss in mice. These effects resolve as the fungal infection clears, suggesting potential links between fungal infections and cognitive function.

Area of Science:

  • Neuroscience
  • Immunology
  • Infectious Diseases

Background:

  • Bloodborne Candida albicans infections are a growing concern in medicine.
  • Disseminated fungal infections can impact various organ systems, including the brain.

Purpose of the Study:

  • To investigate the effects of low-grade candidemia on cerebral function and immune responses in a mouse model.
  • To understand the neuropathological changes associated with Candida albicans brain infection.

Main Methods:

  • Development of a mouse model for low-grade candidemia via intravenous injection of Candida albicans.
  • Analysis of cerebral inflammation, glial cell activation (microglia, astroglia), and granuloma formation.
  • Assessment of amyloid precursor protein and amyloid beta peptide accumulation in the brain.
  • Measurement of inflammatory cytokine production (IL-1β, IL-6, TNF) and NF-κB activation.
  • Evaluation of cognitive function, specifically memory impairment, and its resolution.

Main Results:

  • Candida albicans infection led to localized cerebritis with fungal-induced glial granulomas.
  • Accumulation of amyloid precursor protein and amyloid beta peptides was observed around fungal aggregates.
  • Central nervous system infection activated NF-κB and induced pro-inflammatory cytokines.
  • Mice exhibited transient memory impairment that resolved upon fungal clearance.
  • Amyloid beta peptides were found to enhance microglial phagocytic and antifungal activity.

Conclusions:

  • Disseminated Candida albicans infection can cause significant neuroinflammation and temporary cognitive deficits.
  • The formation of glial granulomas and alterations in amyloid peptides are key features of this infection model.
  • Further research is needed to explore the long-term consequences of chronic cerebritis on cognitive and immune health.

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