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

Maurice Pasternak1, Saira S Mirza1, Andrew D Paterson2

  • 1Hurvitz Brain Sciences Program, Sunnybrook Research Institute, Toronto, ON, Canada.

Alzheimer'S & Dementia : the Journal of the Alzheimer'S Association
|December 25, 2025
PubMed
Summary
This summary is machine-generated.

The protective TMEM106B-rs1990622 variant slows disease progression in genetic Frontotemporal Lobar Degeneration-Tar DNA binding Protein-43 (FTLD-TDP) phenoconverters. This variant reduces NfL levels, brain atrophy, and cognitive decline, indicating therapeutic potential.

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Area of Science:

  • Neuroscience
  • Genetics
  • Neurology

Background:

  • A common TMEM106B variant (rs1990622) is linked to Frontotemporal Lobar Degeneration-Tar DNA binding Protein-43 (FTLD-TDP) risk.
  • The minor allele G of TMEM106B-rs1990622 protects symptomatic mutation carriers by reducing NfL levels, brain atrophy, and cognitive decline.
  • The protective effect of this variant in phenoconverters (individuals showing disease signs after being mutation carriers) was previously unknown.

Purpose of the Study:

  • To investigate the effect of the TMEM106B-rs1990622 variant on disease progression in genetic FTD phenoconverters.
  • To determine if the protective allele G influences NfL levels, brain atrophy, and cognitive decline in individuals who have converted to a symptomatic phenotype.

Main Methods:

  • Studied 518 participants from the GENetic Frontotemporal dementia Initiative (GENFI), including 21 phenoconverters.
  • Analyzed the interaction between TMEM106B-rs1990622 genotype and phenoconverter status using mixed-effects models.
  • Measured serum NfL levels, cognitive function (MMSE, attention, processing speed, executive function, language, CBI), and brain volumetry (MRI).

Main Results:

  • In phenoconverters, the protective allele G significantly reduced the rate of serum NfL accumulation (p < 10-8).
  • Carriers of the protective allele showed slower rates of atrophy in fronto-orbital regions and the insular cortex.
  • Cognitive decline was significantly slower in multiple domains, including general cognition, attention, processing speed, executive function, language, and behavioral symptoms (all p < 0.01).

Conclusions:

  • The TMEM106B-rs1990622 protective variant significantly influences disease progression in genetic FTD phenoconverters.
  • The variant impacts NfL levels, brain atrophy, and cognitive decline, suggesting a broad protective mechanism.
  • This variant holds potential as a therapeutic target for FTD.