Cited by 72Alzheimer's disease research and treatmentsNeuroinflammation and Neurodegeneration MechanismsTelomeres, Telomerase, and Senescence

The novel vaccine peptide GV1001 effectively blocks β-amyloid toxicity by mimicking the extra-telomeric functions of human telomerase reverse transcriptase

Park, Hyun-Hee, Lee, Kyu-Yong, Kim, Sangjae, Lee, Jessica Woojin, Choi, Na-Young, Lee, Eun-Hye, Lee, Young Joo, Lee, Sang-Hun +1 more·2014·Neurobiology of Aging

Abstract

GV1001 is a 16-amino-acid vaccine peptide derived from the human telomerase reverse transcriptase sequence. We investigated the effects of GV1001 against β-amyloid (Aβ) oligomer-induced neurotoxicity in rat neural stem cells (NSCs). Primary culture NSCs were treated with several concentrations of GV1001 and/or Aβ₂₅₋₃₅ oligomer for 48 hours. GV1001 protected NSCs against the Aβ₂₅₋₃₅ oligomer in a concentration-dependent manner. Aβ₂₅₋₃₅ concentration dependently decreased viability, proliferation, and mobilization of NSCs and GV1001 treatment restored the cells to wild-type levels. Aβ₂₅₋₃₅ increased free radical levels in rat NSCs while combined treatment with GV1001 significantly reduced these levels. In addition, GV1001 treatment of Aβ₂₅₋₃₅-injured NSCs increased the expression level of survival-related proteins, including mitochondria-associated survival proteins, and decreased the levels of death and inflammation-related proteins, including mitochondria-associated death proteins. Together, these results suggest that GV1001 possesses neuroprotective effects against Aβ₂₅₋₃₅ oligomer in NSCs and that these effects are mediated through mimicking the extra-telomeric functions of human telomerase reverse transcriptase, including the induction of cellular proliferation, anti-apoptotic effects, mitochondrial stabilization, and anti-aging and anti-oxidant effects.

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Crossref · 10.1016/j.neurobiolaging.2013.12.015

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  • In rat neuronal stem cells, GV1001 blocked Aβ oligomer-induced toxicity and increased the survival of neuronal cells exposed to oxidative stress.

    “In rat neuronal stem cells, GV1001 blocked Aβ oligomer-induced toxicity and increased the survival of neuronal cells exposed to oxidative stress [91,92].”

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Authors
Park, H.-H., Lee, K.-Y., Kim, S., Lee, J. W., Choi, N.-Y., Lee, E.-H., Lee, Y. J., Lee, S.-H., & Koh, S.-H.
Affiliations
  • Hanyang University Guri Hospital (KR)
  • GemVax & KAEL (South Korea) (KR)
  • Hanyang University (KR)
Corresponding author
Koh, Seong-Ho
Venue
Neurobiology of Aging
Publisher
Elsevier BV
Published
2014-06
Volume
35
Issue
6
Pages
1255-1274
ISSN
0197-4580 (ISSN-L)
OpenAlex
W2028466425
Cited by
72
References
46
Citations by year
2026: 6 · 2025: 7 · 2024: 6 · 2023: 10 · 2022: 3 · 2021: 10 · 2020: 4 · 2019: 6 · 2018: 6 · 2017: 4 · 2016: 4 · 2015: 5 · 2013: 1
FWCI
2.89
Type
journal article
Language
en
Open access
closed
Locations
  • Neurobiology of Aging (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Korea Science and Engineering Foundation
  • Ministry of Education, Science and Technology (2007–04717)
  • National Research Foundation of Korea
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
Keywords
GV1001, human telomerase reverse transcriptase, amyloid-beta oligomers, amyloid beta 25-35, neuroprotection, neural stem cells, neurotoxicity, apoptosis, mitochondrial function, oxidative stress, anti-aging, Alzheimer's disease
MeSH terms
Animals, Antioxidants, Cell Movement, Cell Survival, Cells, Cultured, Dose-Response Relationship, Drug, Humans, Peptide Fragments, Amyloid beta-Peptides, Apoptosis, Telomerase, Mitochondrial Proteins, Cell Proliferation, Rats, Neuroprostanes, Neural Stem Cells

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