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

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Area of Science:

  • Neuroscience
  • Genetics
  • Metabolism

Background:

  • The enzyme indoleamine-2,3-dioxygenase (IDO1) is implicated in Alzheimer's disease (AD) pathogenesis.
  • IDO1 activity affects brain metabolism and neuronal support, potentially worsening AD pathologies.
  • The impact of IDO1 genetic variations on AD remains unclear.

Purpose of the Study:

  • To investigate the association between IDO1 single nucleotide polymorphism (SNP) carriership and metabolic disruptions in individuals with AD.
  • To determine if IDO1 SNP carriership influences cognitive decline and Alzheimer's disease biomarkers.

Main Methods:

  • Assessed 619 individuals from the ADNI cohort using FDG-PET, IDO1 genotyping, CSF biomarkers, and cognitive tests.
  • Assigned SNP haplotypes for five IDO1 SNPs and analyzed their association with brain metabolism using generalized linear mixed-models.
  • Examined interactions with APOE4 and associations with cognitive decline and CSF biomarkers.

Main Results:

  • A common IDO1 SNP haplotype (10011) was identified, present in 15.5% of participants.
  • This haplotype correlated with altered brain glucose metabolism (hypermetabolism in cognitively unimpaired, hypometabolism in cognitively impaired individuals).
  • Cognitively impaired carriers showed temporal hypometabolism, exacerbated by APOE4, and severe cognitive impairment linked to elevated CSF pTau181 and GAP43.

Conclusions:

  • This study provides the first in vivo clinical evidence linking an IDO1 SNP to exacerbated brain hypometabolism in AD.
  • IDO1 SNP carriership is associated with worsened cognitive decline and specific metabolic alterations in Alzheimer's disease.