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Alzheimer's Imaging Consortium.

Laura Alejandra Ramirez Tirado1, Ann D Cohen1,2,3,4,5, C Elizabeth Shaaban1,3

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Summary
This summary is machine-generated.

Peripheral inflammation and astrogliosis synergistically impact Alzheimer's disease markers. Higher inflammation correlated with less amyloid accumulation but increased vascular damage and neurodegeneration in older adults.

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Area of Science:

  • Neuroscience
  • Immunology
  • Gerontology

Background:

  • Systemic inflammation and astrogliosis are key factors in Alzheimer's disease (AD).
  • Investigating the combined impact of peripheral inflammation and astrogliosis on AD pathology is crucial.

Purpose of the Study:

  • To evaluate the synergistic effects of peripheral inflammation and astrogliosis on beta-amyloid (Aβ) burden, vascular markers, and neurodegeneration in the Alzheimer's disease spectrum.
  • To analyze the relationship between specific inflammatory markers and astrogliosis with AD-related pathologies.

Main Methods:

  • Utilized data from the Ginkgo Evaluation of Memory Study, including PiB-PET scans and immunoassay measurements of GFAP, NfL, and peripheral inflammatory markers (CRP, sCD14, TNF-R1, TNF-R2).
  • Employed negative binomial regression models, adjusting for relevant covariates, to assess interactions between astrogliosis and peripheral inflammation on Aβ accumulation, white matter lesion (WML) volume, and neurodegeneration (NfL).

Main Results:

  • Significant synergistic effects were observed between astrogliosis (GFAP) and peripheral inflammation (CRP, TNFR1, TNFR2) on white matter lesions and neurodegeneration.
  • A negative interaction between GFAP and CRP was found to slow Aβ accumulation, particularly in individuals with high sCD14 and existing Aβ positivity.
  • Higher GFAP levels were associated with increased WML volume, and interactions with inflammatory markers exacerbated this effect.

Conclusions:

  • In individuals aged 85 and older, peripheral inflammation markers (CRP, TNFR1, TNFR2) demonstrated synergistic effects with astrogliosis.
  • These combined effects led to reduced Aβ accumulation, increased vascular burden, and accelerated neurodegeneration, especially in participants with existing Aβ pathology.
  • The findings suggest that increased inflammation may accelerate AD pathogenesis, potentially reaching the amyloid asymptote faster and slowing Aβ accumulation.