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Alzheimer's Imaging Consortium.

Laura Alejandra Ramirez Tirado1, Ann D Cohen1,2,3, C Elizabeth Shaaban1,2

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Summary
This summary is machine-generated.

Peripheral inflammation markers (TNFR1, TNFR2) and astrogliosis (GFAP) interact synergistically to increase Alzheimer's disease (AD) dementia risk and mortality in individuals with amyloid-beta plaques (Aβ+). This highlights a combined effect on AD progression.

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Area of Science:

  • Neuroscience
  • Immunology
  • Gerontology

Background:

  • Tumor necrosis factor receptor 1 (TNFR1) and TNFR2, along with astrogliosis, have shown synergistic effects on vascular burden and neurodegeneration in amyloid-beta positive (Aβ+) individuals.
  • Peripheral inflammation and astrogliosis interactions require further investigation regarding their impact on Alzheimer's disease (AD) dementia incidence and mortality.

Purpose of the Study:

  • To assess the combined effects of peripheral inflammation (TNFR1, TNFR2) and astrogliosis (GFAP) on the incidence of AD dementia and mortality.
  • To test the hypothesis that synergistic interactions between astrogliosis and peripheral inflammation increase dementia risk and mortality, particularly in Aβ+ participants.

Main Methods:

  • Utilized data from the Gingko Evaluation of Memory (GEM) study, including PiB-PET scans, GFAP, and peripheral inflammatory markers (TNFR1, TNFR2).
  • Employed Cox proportional hazards models, adjusting for age, sex, education, APOEε4, cystatin C, and baseline Aβ status, to evaluate associations with AD dementia incidence and mortality.

Main Results:

  • Aβ+ status was linked to increased dementia risk (HR: 1.73).
  • While high TNFR1 or TNFR2 alone did not significantly increase dementia risk, significant additive and multiplicative interactions were observed between GFAP and TNFR1 (HR: 4.55) and GFAP and TNFR2 (HR: 4.07) in Aβ+ participants.
  • High TNFR1 levels (HR: 1.50) were associated with increased mortality, and synergistic effects on mortality were found between GFAP and TNFR2 in Aβ+ individuals.

Conclusions:

  • The interaction between glial fibrillary acidic protein (GFAP) and tumor necrosis factor receptors (TNFR1, TNFR2) is clinically significant for AD dementia progression.
  • These combined inflammatory and astrogliosis markers predict mortality risk in Aβ+ individuals, suggesting a complex interplay in AD pathogenesis.