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Basic Science and Pathogenesis.

Hongjun Fu1, Tae Yeon Kim2, Diana M Acosta1

  • 1The Ohio State University, Columbus, OH, USA.

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Summary
This summary is machine-generated.

Ectodermal-neural cortex 1 (ENC1) interacts with tau, enhancing its clearance via the autophagy-lysosome pathway (ALP). Reduced ENC1 impairs tau clearance and promotes tau propagation in Alzheimer's disease models.

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genetics

Background:

  • Higher ectodermal-neural cortex 1 (ENC1) RNA levels correlate with preserved cognition.
  • Reduced ENC1 mRNA is observed in Alzheimer's disease (AD) brains.
  • ENC1 is a hub gene regulating tau homeostasis.

Purpose of the Study:

  • Investigate the relationship between ENC1 and tau.
  • Determine if ENC1 enhances tau clearance via the autophagy-lysosome pathway (ALP).
  • Assess ENC1's role in inhibiting tau propagation.

Main Methods:

  • Co-immunoprecipitation and Duolink assays to detect ENC1-tau interaction.
  • Stereotaxic injection of AAV8-CaMKIIa-Cre in ENC1flox/flox mice to knock down ENC1 in excitatory neurons (ENs).
  • Utilized autophagy reporter mice (TRGL6) and tau propagation reporter viruses to measure autophagy dynamics and tau spread.

Main Results:

  • ENC1 interacts with total and pathological tau, with increased interaction in AD brains.
  • ENC1 knockdown in ENs impaired ALP, reducing autolysosomes and increasing autophagosomes.
  • ENC1 knockdown promoted tau propagation in mouse models, evidenced by increased tau in recipient neurons.

Conclusions:

  • ENC1 is a novel regulator of tau protein homeostasis.
  • ENC1 modulates tau clearance and propagation, likely through ALP regulation.