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Dried Blood Spot Collection of Health Biomarkers to Maximize Participation in Population Studies
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Biomarkers.

Christian Limberger1, João Pedro Ferrari-Souza1, Marco Antônio De Bastiani1

  • 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 25, 2025
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Summary
This summary is machine-generated.

This study found that a specific indoleamine-2,3-dioxygenase (IDO1) gene variant is linked to altered brain metabolism and faster cognitive decline in Alzheimer's disease (AD) patients. IDO1 SNP carriership exacerbates hypometabolism and worsens AD progression.

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Area of Science:

  • Neuroscience
  • Genetics
  • Metabolism

Background:

  • Indoleamine-2,3-dioxygenase (IDO1) is upregulated in Alzheimer's disease (AD) astrocytes.
  • IDO1 converts tryptophan to kynurenine, suppressing immune responses and impairing astrocytic glycolysis, reducing neuronal support.
  • IDO1 activity exacerbates AD pathologies by disrupting brain metabolism.

Purpose of the Study:

  • To investigate the functional implications of IDO1 gene single nucleotide polymorphisms (SNPs) in AD.
  • To determine if IDO1 SNP carriership contributes to metabolic disruptions across the AD continuum.

Main Methods:

  • Assessed 619 individuals (cognitively unimpaired and impaired) from ADNI with FDG-PET, IDO1 genotyping, CSF biomarkers, and cognitive data.
  • Assigned SNP haplotypes for five IDO1 SNPs and analyzed their association with brain metabolism using generalized linear mixed-models.
  • Tested the most impactful haplotype for interactions with APOE4 and associations with cognitive decline and CSF biomarkers.

Main Results:

  • A frequent IDO1 SNP haplotype (10011) was identified, associated with altered brain glucose metabolism (hypermetabolism in unimpaired, hypometabolism in impaired individuals).
  • Cognitively impaired carriers of the 10011 haplotype showed temporal hypometabolism, worsened by APOE4, and severe cognitive impairment.
  • Glucose hypometabolism correlated with elevated CSF pTau181 and GAP43 levels.

Conclusions:

  • This study provides the first in vivo clinical evidence linking an IDO1 SNP to exacerbated brain hypometabolism in AD.
  • IDO1 SNP carriership worsens cognitive decline in individuals with Alzheimer's disease.