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Basic Science and Pathogenesis.

Sally A Frautschy1,2, Kapil Manglani2,3, Xiaohong Zuo1,4

  • 1Veterans Greater Los Angeles Healthcare System, Los Angeles, CA, USA.

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

The SARS-CoV-2 spike protein exacerbates Alzheimer's disease (AD) pathology and complement activation in rats, particularly when hypertension or ApoE4 is present. This highlights potential mechanisms for Long Covid neurological symptoms in at-risk populations.

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Area of Science:

  • Neuroscience
  • Immunology
  • Pathology

Background:

  • Persistent symptoms (Long Covid) affect 7% of COVID-19 survivors.
  • SARS-CoV-2 spike protein binds ACE2 receptors, activating complement pathways.
  • Long Covid patients exhibit elevated AD biomarkers and neuroinflammation.

Purpose of the Study:

  • To investigate the modulatory effects of hypertension and ApoE4 on the S1 spike protein response in Alzheimer's disease (AD) rat models.
  • To explore the link between spike protein exposure and AD pathology, white matter damage, and complement activation.

Main Methods:

  • Utilized AD and mixed AD (AD with cerebral small vessel disease) rat models, with and without ApoE4.
  • Administered recombinant S1 protein and assessed executive function, AD pathology, white matter damage, and complement activation.
  • Developed high-throughput plasma assays for vascular and CNS complement activation in rat models and human Neuro-Covid patients.

Main Results:

  • S1 protein increased amyloid pathology, ptau217, and complement activation (C3, C5b-9) independently of ApoE or hypertension.
  • Hypertension and ApoE4 synergized to worsen spike-induced vascular pathology and leukocyte adhesion.
  • Spike protein induced executive dysfunction, white matter damage, and complement activation, potentiated by pre-existing hypertension.

Conclusions:

  • Spike protein robustly increases AD pathology and complement activation, causing synapse loss and blood-brain barrier damage in rats with pre-existing AD and vascular conditions.
  • These findings are relevant to a significant portion of the aging population with comorbidities.
  • Development of scalable assays for Neuro-Covid complement activation could aid in treatment strategies.