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Alzheimer's Imaging Consortium.

Catarina Tristão-Pereira1,2, David Fernando Aguillón Niño3, Ana Y Baena4

  • 1Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.

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Summary
This summary is machine-generated.

In autosomal-dominant Alzheimer's disease (AD), brain glucose hypometabolism measured by 18F-fluorodeoxyglucose (FDG) PET reflects both reactive astrogliosis and neuronal injury. This suggests a more complex interpretation of FDG-PET imaging in early AD detection.

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Area of Science:

  • Neuroimaging
  • Biomarkers
  • Neurodegenerative Diseases

Background:

  • Cerebral glucose hypometabolism (18F-fluorodeoxyglucose PET) is a hallmark of Alzheimer's disease (AD).
  • Metabolic changes in AD are complex, with astrocytes contributing significantly to the FDG-PET signal.
  • This study investigates plasma glial fibrillary acidic protein (GFAP) and neurofilament light chain (NfL) contributions to FDG-PET in autosomal-dominant AD.

Purpose of the Study:

  • To investigate the differential contribution of plasma GFAP and NfL to FDG-PET in autosomal-dominant AD.
  • To explore the relationship between astrogliosis, neuronal injury, and cerebral metabolism in early AD.
  • To refine the interpretation of FDG-PET imaging in AD.

Main Methods:

  • Included 40 Presenilin-1 E280A mutation carriers and 37 controls from the COLBOS Biomarkers Study.
  • Quantified plasma GFAP and NfL; processed FDG-PET uptake across Freesurfer regions.
  • Used Spearman correlation, Lasso regression, and mediation analysis to assess biomarker associations with FDG uptake.

Main Results:

  • Mutation carriers showed higher plasma GFAP and NfL than controls.
  • Both GFAP and NfL correlated negatively with FDG uptake in carriers, particularly in temporo-parietal regions and the hippocampus.
  • Plasma GFAP, but not NfL, remained significantly associated with global FDG uptake in Lasso regression, showing an independent effect.

Conclusions:

  • FDG-PET signal in AD may reflect both reactive astrogliosis and neuronal injury.
  • Reactive astrogliosis impacts hypometabolism independently of neurodegeneration.
  • Vascular or neuroinflammatory mechanisms may contribute to hypometabolism and early AD, necessitating cautious FDG-PET interpretation.