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

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

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

DOI 10.1046/j.1471-4159.2000.0750117.x

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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.

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Authors: Zhu, H., Fu, W., & Mattson, M. P.
Affiliations: University of Kentucky (US)
National Institutes of Health (US)
ORCID: Zhu, Haiyan
Fu, Weiming
Mattson, Mark P.
Venue: Journal of Neurochemistry
Publisher: Wiley
Published: 2000-07
Volume: 75
Issue: 1
Pages: 117-124
ISSN: 0022-3042 (ISSN-L)
1471-4159
DOI: 10.1046/j.1471-4159.2000.0750117.x
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: bronze
doi.org
Licence: onlinelibrary.wiley.com/termsAndConditions#vor (vor, 542 d)
Locations: Journal of Neurochemistry (publishedVersion)
PubMed (publishedVersion)
Topics: Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › 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

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

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