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Replicative cell senescence is a property of cells that allows them to divide a finite number of times throughout the organism's lifespan while preventing excessive proliferation. Replicative senescence is associated with the gradual loss of the telomere — short, repetitive DNA sequences found at the end of the chromosomes. Telomeres are bound by a group of proteins to form a protective cap on the ends of chromosomes. Embryonic stem cells express telomerase — an enzyme that adds...
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Related Experiment Video

Updated: Mar 19, 2026

Telomerase Activity in the Various Regions of Mouse Brain: Non-Radioactive Telomerase Repeat Amplification Protocol TRAP Assay
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Telomerase Activity is Downregulated Early During Human Brain Development.

Abbas Ishaq1,2, Peter S Hanson3,4, Christopher M Morris5,6

  • 1Institute for Cell and Molecular Biosciences, Newcastle University, Newcastle upon Tyne NE1 7RU, UK. A.Ishaq1@newcastle.ac.uk.

Genes
|June 21, 2016
PubMed
Summary
This summary is machine-generated.

Telomerase activity in the human brain decreases early in development, primarily due to reduced telomerase RNA (hTR). Transient increases in a spliced form of hTERT also contribute to this downregulation.

Keywords:
braindevelopmentexpressionhTERT splice-variantshTRneural stem cellstelomerase activity

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genetics

Background:

  • Telomerase activity is crucial for cell proliferation and is tightly regulated during development.
  • Changes in human telomerase reverse transcriptase (hTERT) splice variants are implicated in telomerase regulation.
  • Understanding telomerase dynamics in the developing human brain is essential for insights into neurodevelopment.

Purpose of the Study:

  • To investigate the expression of telomerase components (hTR, wild-type hTERT, α-spliced hTERT) during human fetal brain development.
  • To correlate telomerase activity with the expression of these components in the developing and adult brain.
  • To assess the utility of neural precursor stem cells (NPSCs) in modeling these developmental changes.

Main Methods:

  • Quantitative PCR (qPCR) to measure hTR and hTERT splice variant expression.
  • Telomerase activity assay (TRAP) to quantify telomerase function.
  • Analysis of human fetal brain tissue (6-19 pcw) and adult cortices.
  • In vitro differentiation of NPSCs.

Main Results:

  • Telomerase activity decreased early in human brain development (6-17 pcw), correlating strongly with reduced hTR expression.
  • Expression of α-spliced hTERT increased between 10-19 pcw, while wild-type hTERT remained stable.
  • No significant expression differences were observed between young and old adult cortices.
  • In vitro differentiated NPSCs showed decreased telomerase activity but not significant changes in associated gene expression, failing to model fetal brain changes.

Conclusions:

  • Decreased hTR levels are a primary driver of telomerase downregulation in the early fetal brain.
  • A transient increase in α-spliced hTERT may also contribute to telomerase downregulation during early human brain development.
  • Neural precursor stem cells may not fully recapitulate the in vivo mechanisms of telomerase regulation during fetal brain development.