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Basic Science and Pathogenesis.

Caitlin Newman1, Marlene Tejeda2, John J Farrell3

  • 1Boston University, Boston, MA, USA.

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

Herpes simplex virus type 1 (HSV-1) DNA was linked to decreased tau levels in several brain regions, suggesting a potentially protective role against tau buildup in Alzheimer's Disease (AD). Further research is needed to understand this complex relationship.

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Area of Science:

  • Neuroscience
  • Virology
  • Genetics

Background:

  • Herpes simplex virus type 1 (HSV-1) infection is implicated in Alzheimer's Disease (AD) pathogenesis.
  • Latent herpes infections may influence amyloid and tau pathology, but the precise link to HSV-1 presence and protein deposition is unclear.

Purpose of the Study:

  • To investigate the association between HSV-1 DNA quantity and amyloid-β and tau deposition in the brain.
  • To explore the relationship between HSV-1 presence and neurodegenerative markers in Alzheimer's Disease.

Main Methods:

  • Whole-genome sequencing data from the Alzheimer's Disease Sequencing Project (ADSP) were analyzed for HSV-1 DNA.
  • Amyloid-β and tau PET imaging data were correlated with HSV-1 DNA levels using linear regression models.
  • Participants included cases and cognitively normal controls from ADNI and the Wisconsin Registry for Alzheimer's Prevention.

Main Results:

  • HSV-1 DNA was detected in 300 participants.
  • No significant association was found between HSV-1 DNA and amyloid PET metrics.
  • HSV-1 DNA showed a significant association with decreased tau levels in multiple brain regions, including the hippocampus, cerebral white matter, amygdala, CSF, and caudate.

Conclusions:

  • The study suggests a complex interaction between HSV-1 and tau pathology, potentially indicating a protective effect of HSV-1 against tau accumulation in certain brain areas.
  • The findings highlight the need for further investigation into the mechanisms governing the HSV-1-tau relationship and its implications for neurodegeneration.