Cited by 175Alzheimer's disease research and treatmentsTelomeres, Telomerase, and SenescenceNeuroinflammation and Neurodegeneration Mechanisms

The Catalytic Subunit of Telomerase Protects Neurons Against Amyloid β‐Peptide‐Induced Apoptosis

Open access
Zhu, Haiyan, Fu, Weiming, Mattson, Mark P.·2000·Journal of Neurochemistry

Abstract

Abstract : The catalytic subunit of telomerase (TERT) is a specialized reverse transcriptase that has been associated with cell immortalization and cancer. It was reported recently that TERT is expressed in neurons throughout the brain in embryonic and early postnatal development, but is absent from neurons in the adult brain. We now report that suppression of TERT levels and function in embryonic mouse hippocampal neurons in culture using antisense technology and the telomerase inhibitor 3' ‐azido‐2' 3' ‐dideoxythymidine significantly increases their vulnerability to cell death induced by amyloid β‐peptide, a neurotoxic protein believed to promote neuronal degeneration in Alzheimer's disease. Neurons in which TERT levels were reduced exhibited increased levels of oxidative stress and mitochondrial dysfunction following exposure to amyloid β‐peptide. Overexpression of TERT in pheochromocytoma cells resulted in decreased vulnerability to amyloid β‐peptide‐induced apoptosis. Our findings demonstrate a neuroprotective function of TERT in an experimental model relevant to Alzheimer's disease, and suggest the possibility that restoration of TERT expression in neurons in the adult brain may protect against age‐related neurodegeneration.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1046/j.1471-4159.2000.0750117.x

Cites

62 of 62 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Telomerase appears to protect against amyloid-β-induced cell death in embryonic mouse hippocampal neurons in vitro.

    “and against amyloid-β-induced cell death in embryonic mouse hippocampal neurons in vitro166”

    From Telomere dysfunction in ageing and age-related diseases (2022) · cites this paper as [166]

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

Flagged first, then by citations

2 of the 64 references couldn’t be matched to a known paper.

Research works printed but not linked: 1

  1. [19]19. Greider C. W. (1998) Telomerase activity, cell proliferation, and can- cer. Proc. Natl. Acad. Sci. USA 95, 90 -92.

Cited by

Sorted by citations

Authors
Zhu, H., Fu, W., & Mattson, M. P.
Affiliations
  • University of Kentucky (US)
  • National Institutes of Health (US)
Venue
Journal of Neurochemistry
Publisher
Wiley
Published
2000-07
Volume
75
Issue
1
Pages
117-124
ISSN
  • 0022-3042 (ISSN-L)
  • 1471-4159
OpenAlex
W2071245320
Cited by
175
References
64
Citations by year
2024: 2 · 2023: 3 · 2022: 4 · 2021: 5 · 2020: 7 · 2019: 5 · 2018: 6 · 2017: 6 · 2016: 7 · 2015: 8 · 2014: 7 · 2013: 10 · 2012: 3
FWCI
7.98
Type
journal article
Language
en
Open access
Locations
  • Journal of Neurochemistry (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords
telomerase reverse transcriptase, amyloid-beta, neuronal apoptosis, neuroprotection, Alzheimer's disease, oxidative stress, mitochondrial dysfunction, hippocampal neurons, telomerase inhibitors, zidovudine, age-related neurodegeneration
MeSH terms
Alzheimer Disease, Animals, Cells, Cultured, DNA-Binding Proteins, Embryo, Mammalian, Enzyme Inhibitors, Hippocampus, Immunohistochemistry, Mitochondria, Neurons, RNA, Gene Expression, Amyloid beta-Peptides, Oligonucleotides, Antisense, PC12 Cells, Apoptosis, Oxidative Stress, Telomerase, Catalytic Domain, Mice, Rats

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review