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Basic Science and Pathogenesis.

Joseph Bradley1,2, Daniel Western1,2, Ciyang Wang1,2

  • 1Department of Psychiatry, Washington University School of Medicine, St. Louis, MO, USA.

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|December 24, 2025
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Summary
This summary is machine-generated.

This study identifies novel genetic loci and genes for early-onset Alzheimer disease (EOAD), revealing shared and unique genetic factors compared to late-onset AD. Findings may improve prediction models and therapeutic targets for EOAD.

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Area of Science:

  • Genetics
  • Neuroscience
  • Medical Research

Background:

  • Alzheimer Disease (AD) is a polygenic dementia with early-onset (EOAD) cases presenting before 65.
  • Approximately 90% of EOAD cases lack identified pathogenic mutations, indicating unknown genetic factors.

Purpose of the Study:

  • To identify novel genetic loci associated with early-onset Alzheimer Disease (EOAD).
  • To compare the genetic architecture of EOAD with late-onset Alzheimer Disease (LOAD).
  • To nominate novel functional genes contributing to EOAD pathogenesis.

Main Methods:

  • Genome-wide association study (GWAS) and trans-ancestry meta-analysis across European, African, and East Asian ancestries.
  • QTL mapping and in-silico annotation to identify functional genes at genome-wide significant loci.
  • Polygenic Risk Score (PRS) and Linkage Disequilibrium (LDSC) analyses to compare EOAD and LOAD genetic architecture.

Main Results:

  • Identified 15 genome-wide significant loci, including 8 novel loci for EOAD.
  • Nominated four novel functional genes (CDH12, FOLH1, ALG10B, LRRC25) implicated in microglial activation and signaling pathways.
  • Demonstrated strong genetic correlation between EOAD and LOAD, with significant PRS association.

Conclusions:

  • EOAD shares genetic factors with LOAD but also possesses unique genetic underpinnings.
  • Novel identified genes and pathways offer potential for improved EOAD prediction models.
  • Findings pave the way for targeted therapeutic strategies for early-onset Alzheimer Disease.