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Basic Science and Pathogenesis.

Marco De Bastiani1, Christian Limberger1, Débora Guerini de Souza1,2

  • 1Universidade Federal do Rio Grande do Sul, Porto Alegre, Rio Grande do Sul, Brazil.

Alzheimer'S & Dementia : the Journal of the Alzheimer'S Association
|December 24, 2025
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Summary
This summary is machine-generated.

Genetic variants influencing PLEK gene expression are linked to brain glucose metabolism changes in Alzheimer's disease (AD). This suggests a connection between immune response proteins and AD pathology, warranting further investigation.

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Area of Science:

  • Neurogenetics
  • Molecular Psychiatry
  • Neuroimaging

Background:

  • Alzheimer's disease (AD) is a complex neurodegenerative disorder influenced by genetic factors.
  • Expression quantitative trait loci (eQTL) mapping is crucial for understanding how genetic variants regulate gene expression and disease mechanisms.
  • This study investigates the interplay between genetic variants, blood gene expression, and brain metabolism in AD.

Purpose of the Study:

  • To explore the association between genetic variants, blood gene expression, and brain glucose metabolism using FDG-PET imaging.
  • To identify specific genetic variants and their regulatory effects on gene expression that correlate with metabolic changes in the brain.

Main Methods:

  • Analysis of genomic and blood transcriptomic data from 746 individuals in the ADNI dataset.
  • eQTL mapping to identify significant gene-SNP associations, controlling for age and sex.
  • Voxel-wise regression analysis of FDG-PET data to assess the impact of gene-SNP interactions on brain glucose metabolism.

Main Results:

  • Over 5,000 SNPs significantly associated with the expression of 217 genes were identified.
  • Carriers of a specific PLEK gene variant (rs8761), associated with gene downregulation, showed increased glucose metabolism (hypermetabolism) in frontal and temporal cortices.
  • Another PLEK variant (rs1063479) linked to gene upregulation did not show significant FDG-PET changes.

Conclusions:

  • The PLEK gene, encoding a plasma protein involved in immune response and expressed in glial cells, shows variants associated with brain glucose metabolism.
  • This suggests a novel link between immune-related plasma proteins and brain metabolism in the context of AD.
  • Further research is needed to elucidate the mechanisms underlying the role of PLEK in brain metabolism and its implications for AD pathogenesis.