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Summary
This summary is machine-generated.

Genetic variations in the TMEM106B gene influence neurodegenerative disease risk. Specific haplotypes, like HAB and Hab, show distinct associations with Alzheimer

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Area of Science:

  • Genetics
  • Neuroscience
  • Molecular Biology

Background:

  • Genome-wide association studies (GWAS) have implicated TMEM106B variants in neurodegenerative disease susceptibility.
  • The precise causal genetic elements within the TMEM106B locus remain incompletely understood.

Purpose of the Study:

  • To identify specific haplotypes within the TMEM106B locus associated with Alzheimer's disease (AD).
  • To characterize the structural variations and molecular features of these haplotypes.
  • To elucidate the differential effects of TMEM106B haplotypes on disease risk and TMEM106B protein levels.

Main Methods:

  • Genotyping data from 5,792 Alzheimer's disease cases and controls were analyzed using COJO.
  • Long-read sequencing of 513 individuals was employed to annotate haplotypes with structural variations.
  • Proteomic analysis of temporal cortex tissues (n=182) assessed TMEM106B C-terminal peptide abundance.

Main Results:

  • Four major TMEM106B haplotypes (HA/Ha and HB/Hb) were identified, combining into HAB, HaB, Hab, and HAb.
  • The HAB haplotype (AluYb8 + 185-Threonine) is associated with increased AD risk, while the Hab haplotype (SVs + 185-Serine) is protective.
  • Proteomic analysis revealed altered TMEM106B C-terminal peptide levels correlating with haplotype-specific disease risk.

Conclusions:

  • The association of the TMEM106B locus with neurodegenerative diseases is driven by the combined effects of multiple distinct haplotypes.
  • Specific TMEM106B haplotypes confer differential risks and protective effects against Alzheimer's disease, mediated by structural variations and sequence alleles.