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Related Experiment Videos

Tau Activates Transposable Elements in Alzheimer's Disease.

Caiwei Guo1, Hyun-Hwan Jeong2, Yi-Chen Hsieh2

  • 1Department of Neuroscience, Baylor College of Medicine, Houston, TX 77030, USA; Jan and Dan Duncan Neurologic Research Institute, Texas Children's Hospital, Houston, TX 77030, USA.

Cell Reports
|June 7, 2018
PubMed
Summary

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Transposable elements (TEs) and genomic instability are linked to Alzheimer's disease (AD). This study shows Tau pathology activates TEs in both human brains and fruit fly models, suggesting a role in AD progression.

Area of Science:

  • Neuroscience
  • Genetics
  • Molecular Biology

Background:

  • Aging and neurodegenerative diseases, including Alzheimer's disease (AD), exhibit genomic instability in neurons.
  • Aberrant activation and mobilization of transposable elements (TEs) are key features of this genomic instability.
  • The role of Tau pathology in TE activation within AD remains an active area of investigation.

Purpose of the Study:

  • To investigate the association between Tau pathology and transposable element (TE) activation in Alzheimer's disease (AD).
  • To determine if Tau is sufficient to induce TE activation using model organisms.
  • To elucidate the mechanisms linking TE activation and genomic instability to Tau-mediated AD pathogenesis.

Main Methods:

  • RNA sequencing analysis of 636 human postmortem brain tissues to assess TE expression.
Keywords:
AluAlzheimer's diseaseERVLINE1MAPTRNA sequencingchromatingenomic instabilityneurodegenerationretrotransposon

Related Experiment Videos

  • Analysis of chromatin signatures at specific genomic loci associated with Tau pathology.
  • Utilized Drosophila melanogaster models expressing human wild-type or mutant Tau to profile retrotransposon activity.

    • Main Results:

    • Differential expression of retrotransposons was observed in human brains, correlating with neurofibrillary tangle burden.
    • Evidence of global TE transcriptional activation, particularly Long Interspersed Nuclear Element 1 and endogenous retroviruses, was found.
    • Tau expression in Drosophila induced heterogeneous, age- and genotype-dependent activation of TE expression.

    Conclusions:

    • Tau pathology is implicated in the activation of transposable elements (TEs) in Alzheimer's disease.
    • TE activation and subsequent genomic instability may contribute to Tau-mediated neurodegeneration in AD.
    • Findings highlight a novel mechanism involving TEs in AD pathogenesis, offering potential therapeutic targets.