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Basic Science and Pathogenesis.

Gabriela Lazzarotto1, Lidia Emmanuela Wiazowski Spelta2, Cleinando Clemente da Silva Vera2

  • 1UFRGS, Porto Alegre, Brazil.

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This study used PET imaging in a rat model to track Alzheimer's disease (AD) biomarkers over time. Results show amyloid deposition, increased glucose metabolism, and glial reactivity, supporting AD progression in animal models.

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Area of Science:

  • Neuroscience
  • Biomarker Discovery
  • Medical Imaging

Background:

  • Alzheimer's disease (AD) diagnosis and monitoring rely on PET tracers for amyloid-beta (Aβ) plaques, glucose metabolism, and glial reactivity.
  • The accuracy of animal models in replicating the temporal progression of AD biomarker abnormalities remains unclear.

Purpose of the Study:

  • To longitudinally evaluate brain Aβ accumulation, glucose metabolism, and glial responses in a rat model of amyloidosis using PET imaging.

Main Methods:

  • Longitudinal PET imaging ([18F]FDG, [11C]PK11195, [11C]PIB) was conducted on wild-type (WT) and TgF344-AD (Tg) rats at 6, 9, 12, and 15 months.
  • Images were co-registered to an MRI template, and standardized uptake values (SUV/SUVR) were calculated.
  • Results were normalized using Z-scores (Z > 2 considered significant).

Main Results:

  • No significant differences were observed between WT and Tg rats at 6 months.
  • By 9 months, Tg rats showed increased Aβ deposition, enhanced glucose metabolism, and heightened glial reactivity.
  • Aβ load and glucose metabolism continued to rise, with fluctuating glial reactivity at 12 and 15 months.

Conclusions:

  • Early Aβ deposition correlates with increased glucose metabolism and glial reactivity, followed by a transient decrease and later resurgence of glial activation.
  • Amyloid deposition triggers both early and late neuroinflammatory responses.
  • Persistent hypermetabolism in models suggests resilience to amyloid pathology, highlighting the value of imaging platforms for studying AD progression in rodent models.