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Telomerase reverse transcriptase (TERT) repression contributes to Alzheimer's disease. Restoring TERT in neurons reduces amyloid-beta, improves cognition, and offers a potential gene therapy for AD.

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Area of Science:

  • Neuroscience
  • Genetics
  • Molecular Biology

Background:

  • Alzheimer's disease (AD) is characterized by amyloid-induced neurodegeneration.
  • Telomerase reverse transcriptase (TERT) plays a crucial role in cellular processes, but its role in AD is not fully understood.

Purpose of the Study:

  • To investigate the role of TERT in Alzheimer's disease pathogenesis.
  • To explore the therapeutic potential of TERT activation in AD.

Main Methods:

  • Studied TERT haploinsufficiency effects on BDNF and amyloid-beta precursor in mouse models.
  • Analyzed epigenetic modifications at the TERT locus in murine and human AD neurons.
  • Engineered AD mouse models with sustained TERT expression in adult neurons.
  • Utilized integrated profiling to elucidate TERT's molecular mechanisms.

Main Results:

  • TERT haploinsufficiency decreased BDNF and increased amyloid-beta precursor.
  • Repressive epigenetic marks accumulated at the TERT locus in AD neurons.
  • Sustained TERT expression in AD mouse models reduced amyloid-beta, improved synaptic morphology, and preserved cognitive function.
  • TERT was found to interact with beta-catenin and RNA polymerase II, upregulating synaptic and learning gene networks.

Conclusions:

  • TERT repression is implicated in amyloid-induced neurodegeneration in Alzheimer's disease.
  • Somatic TERT gene activation is a potential therapeutic strategy for attenuating AD progression and cognitive decline.