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Basic Science and Pathogenesis.

Muralidharan Sargurupremraj1, Sathyaseelan Chakkarai1, Yinan Zheng2

  • 1University of Texas Health Science Center at San Antonio, San Antonio, TX, USA.

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Summary
This summary is machine-generated.

Transposable elements (TEs) influence Alzheimer's disease (AD) risk by altering brain volume and methylation patterns. This study links specific TEs to AD pathology, offering new insights into disease mechanisms.

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Area of Science:

  • Genomics and Epigenetics
  • Neuroscience
  • Computational Biology

Background:

  • Transposable elements (TEs) comprise ~45% of the human genome and can relocate.
  • In vivo studies link TEs to Alzheimer's disease (AD) pathology, but population-scale analysis is challenging due to TE diversity.
  • This study integrates genomic and epigenetic data to explore TE influence on preclinical AD and related dementia (ADRD) risk.

Purpose of the Study:

  • To investigate the role of polymorphic TE insertions (pTEIs) and TE methylation states in AD pathogenesis.
  • To assess the association of pTEIs with brain imaging endophenotypes like hippocampal volume (HV) and total brain volume (TBV).
  • To analyze differential methylation patterns of TEs in AD brains compared to controls.

Main Methods:

  • Utilized multi-omics data from TOPMed and AMP-AD initiatives.
  • Employed machine learning to genotype pTEIs and predict TE methylation states (LINE, SINE, ERVs).
  • Applied whole-genome regression and functional enrichment models to analyze genetic susceptibility and methylation patterns.

Main Results:

  • A common LINE-1 (L1Hs) pTEI near RYR3 was associated with TBV atrophy in cognitively normal individuals.
  • Altered L1Hs methylation patterns were observed in AD brains.
  • Differential methylation of TEs within KDM2B and SPATA5 was linked to HV and cognitive decline.

Conclusions:

  • Integrated genomic and methylation data reveal novel insights into TE involvement in AD pathogenesis and risk.
  • TEs contribute to AD risk through epigenetic modifications and gene regulation.
  • Further research using ChIP-seq data will characterize TE regulatory impact on gene expression.