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Basic Science and Pathogenesis.

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Summary
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Genetic variants in hydrogen sulfide (H2S) pathways are linked to Alzheimer's disease (AD) and related dementias (ADRD). This study provides genetic support for H2S-related genes as therapeutic targets for AD and ADRD.

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Area of Science:

  • Genetics
  • Biochemistry
  • Neuroscience

Background:

  • Hydrogen sulfide (H2S) is a gasotransmitter crucial for homeostasis and a potential therapeutic target for Alzheimer's disease (AD) and related dementias (ADRD).
  • Genetic evidence supporting H2S-related pathways as drug targets is limited.
  • This study investigates the impact of genetic variants in H2S pathways on numerous phenotypes using large-scale biobanks.

Purpose of the Study:

  • To explore the association between genetic variants in H2S synthesis and metabolism genes and various clinical outcomes.
  • To identify potential genetic support for H2S-related pathways as therapeutic targets for AD and ADRD.

Main Methods:

  • Conducted a phenome-wide association study (PheWAS) on eight H2S-related genes in the FinnGen biobank (N=453,733).
  • Utilized single nucleotide polymorphisms (SNPs) associated with gene expression and the Wald ratio estimator to assess genetically predicted gene expression effects.
  • Applied a phenome-wide association threshold (p < 1x10^-5) and employed MAGMA software for polygenic enrichment analysis of H2S-related gene sets.

Main Results:

  • Identified significant associations between H2S-related SNPs and ADRD endpoints, surpassing multiple testing correction.
  • SNP-predicted ETHE1 expression was linked to AD and cardiovascular diseases, while SUOX expression was associated with ADRD, type 1 diabetes, and other metabolic/auto-immune disorders.
  • Found nominal enrichment of genetic risk for cerebrovascular disease and AD in H2S-related gene sets, suggesting polygenic effects.

Conclusions:

  • This study provides the first systematic genetic evidence supporting ETHE1 and SUOX, and H2S pathways, as targets for therapeutic intervention in AD and ADRD.
  • The findings support H2S as a potential modifier of neurocognitive and cerebrovascular pathology.
  • Highlights the utility of network-defined gene set analyses for uncovering system-specific effects in complex diseases.