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Basic Science and Pathogenesis.

Han Zhao1, Haowei Xu2, Junkai Xie1

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Summary
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Researchers developed a novel FRET biosensor to track TDP-43 aggregation in living neurons, a key factor in Alzheimer's disease and related dementias (ADRD). This tool aids in understanding disease progression and identifying therapeutic targets for ADRD.

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Biochemistry

Background:

  • Alzheimer's disease and related dementias (ADRD) affect millions, with TDP-43 pathology increasingly linked to cognitive decline.
  • The molecular mechanisms of TDP-43's role in ADRD are poorly understood due to a lack of tools to monitor its aggregation in living cells.

Purpose of the Study:

  • To engineer a Förster Resonance Energy Transfer (FRET)-based biosensor for detecting TDP-43 aggregation in real-time within living neurons.
  • To utilize this biosensor to investigate the progression of TDP-43 pathology under conditions mimicking aging-related cellular stress.

Main Methods:

  • Engineered a FRET biosensor using various TDP-43 isoforms and linker constructs.
  • Validated biosensor sensitivity using proteostasis stress conditions and preformed TDP-43 fibrils.
  • Transduced the biosensor into human iPSC-derived cortical neurons and monitored FRET signal changes after treatment with aging-mimicking stressors.

Main Results:

  • The FRET biosensor successfully detected TDP-43 aggregation in response to proteostasis stressors.
  • Neurons treated with aging-mimicking compounds showed increased FRET signals, indicating progressive TDP-43 aggregation over time.

Conclusions:

  • Developed a novel FRET biosensor for real-time monitoring of TDP-43 aggregation in living neurons.
  • This tool facilitates the study of TDP-43 pathology dynamics and the identification of disrupted molecular pathways in ADRD.