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Basic Science and Pathogenesis.

Cemal Akmese1, Rodrigo Francisco Tomas1, Huong T Phuong2

  • 1University of Florida, College of Medicine, Gainesville, FL, USA.

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Summary
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Alzheimer's disease brain tissue shows increased poly-glycine-arginine (polyGR) aggregates, particularly linked to vascular factors like hypertension and traumatic brain injury (TBI). This accumulation appears independent of tau pathology, offering new insights into AD.

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Area of Science:

  • Neuroscience
  • Pathology
  • Genetics

Background:

  • Alzheimer's disease (AD) is a neurodegenerative disorder marked by amyloid plaques and tau tangles.
  • Sporadic AD mechanisms are largely unknown, unlike rare familial forms.
  • Recent findings indicate poly-glycine-arginine (polyGR) aggregates in AD brain tissue, associated with tau pathology.

Purpose of the Study:

  • To investigate the association between polyGR aggregate levels and clinical histories in Alzheimer's disease patients.
  • To explore the link between vascular comorbidities, head injuries, and polyGR accumulation in AD.
  • To determine if polyGR accumulation is related to tau pathology in AD.

Main Methods:

  • Autopsy brain tissues from 133 AD cases and 30 controls were analyzed.
  • Immunohistochemistry was used to measure polyGR aggregates in hippocampal sections.
  • Statistical analyses correlated polyGR levels with clinical data, including vascular factors and TBI history.

Main Results:

  • PolyGR accumulation was significantly elevated (9.4-fold) in AD cases compared to controls.
  • In late-onset AD (LOAD), traumatic brain injury (TBI), hypertension, and high cholesterol were associated with increased polyGR staining.
  • These vascular and metabolic risk factors did not significantly affect tau pathology (pTau) levels.

Conclusions:

  • Vascular and metabolic risk factors, including TBI and hypertension, promote polyGR accumulation in Alzheimer's disease.
  • PolyGR accumulation occurs independently of tau (pTau) aggregation in AD.
  • Findings suggest novel molecular pathways linking vascular health to AD pathogenesis.