Skip to main content

Lund University Publications

LUND UNIVERSITY LIBRARIES

Oxidative DNA Damage Signalling in Neural Stem Cells in Alzheimer's Disease

Kieroń, Marcelina ; Żekanowski, Cezary ; Falk, Anna LU and Wężyk, Michalina (2019) In Oxidative Medicine and Cellular Longevity 2019.
Abstract

The main pathological symptoms of Alzheimer's disease (AD) are β-amyloid (Aβ) lesions and intracellular neurofibrillary tangles of hyperphosphorylated tau protein. Unfortunately, existing symptomatic therapies targeting Aβ and tau remain ineffective. In addition to these pathogenic factors, oxidative DNA damage is one of the major threats to newborn neurons. It is necessary to consider in detail what causes neurons to be extremely susceptible to oxidative damage, especially in the early stages of development. Accordingly, the regulation of redox status is crucial for the functioning of neural stem cells (NSCs). The redox-dependent balance, of NSC proliferation and differentiation and thus the neurogenesis process, is controlled by a... (More)

The main pathological symptoms of Alzheimer's disease (AD) are β-amyloid (Aβ) lesions and intracellular neurofibrillary tangles of hyperphosphorylated tau protein. Unfortunately, existing symptomatic therapies targeting Aβ and tau remain ineffective. In addition to these pathogenic factors, oxidative DNA damage is one of the major threats to newborn neurons. It is necessary to consider in detail what causes neurons to be extremely susceptible to oxidative damage, especially in the early stages of development. Accordingly, the regulation of redox status is crucial for the functioning of neural stem cells (NSCs). The redox-dependent balance, of NSC proliferation and differentiation and thus the neurogenesis process, is controlled by a series of signalling pathways. One of the most important signalling pathways activated after oxidative stress is the DNA damage response (DDR). Unfortunately, our understanding of adult neurogenesis in AD is still limited due to the research material used (animal models or post-mortem tissue), providing inconsistent data. Now, thanks to the advances in cellular reprogramming providing patient NSCs, it is possible to fill this gap, which becomes urgent in the light of the potential of their therapeutic use. Therefore, a decent review of redox signalling in NSCs under physiological and pathological conditions is required. At this moment, we attempt to integrate knowledge on the influence of oxidative stress and DDR signalling in NSCs on adult neurogenesis in Alzheimer's disease.

(Less)
Please use this url to cite or link to this publication:
author
; ; and
publishing date
type
Contribution to journal
publication status
published
subject
keywords
Alzheimer Disease/genetics, Animals, DNA Damage, Humans, Neural Stem Cells/metabolism, Oxidative Stress/genetics, Signal Transduction
in
Oxidative Medicine and Cellular Longevity
volume
2019
article number
2149812
pages
10 pages
publisher
Hindawi Limited
external identifiers
  • scopus:85075761144
  • pmid:31814869
ISSN
1942-0900
DOI
10.1155/2019/2149812
language
English
LU publication?
no
id
1bf39b33-6b84-414d-9055-f918b4cda0d1
date added to LUP
2021-08-09 14:39:56
date last changed
2024-03-23 07:15:32
@article{1bf39b33-6b84-414d-9055-f918b4cda0d1,
  abstract     = {{<p>The main pathological symptoms of Alzheimer's disease (AD) are β-amyloid (Aβ) lesions and intracellular neurofibrillary tangles of hyperphosphorylated tau protein. Unfortunately, existing symptomatic therapies targeting Aβ and tau remain ineffective. In addition to these pathogenic factors, oxidative DNA damage is one of the major threats to newborn neurons. It is necessary to consider in detail what causes neurons to be extremely susceptible to oxidative damage, especially in the early stages of development. Accordingly, the regulation of redox status is crucial for the functioning of neural stem cells (NSCs). The redox-dependent balance, of NSC proliferation and differentiation and thus the neurogenesis process, is controlled by a series of signalling pathways. One of the most important signalling pathways activated after oxidative stress is the DNA damage response (DDR). Unfortunately, our understanding of adult neurogenesis in AD is still limited due to the research material used (animal models or post-mortem tissue), providing inconsistent data. Now, thanks to the advances in cellular reprogramming providing patient NSCs, it is possible to fill this gap, which becomes urgent in the light of the potential of their therapeutic use. Therefore, a decent review of redox signalling in NSCs under physiological and pathological conditions is required. At this moment, we attempt to integrate knowledge on the influence of oxidative stress and DDR signalling in NSCs on adult neurogenesis in Alzheimer's disease.</p>}},
  author       = {{Kieroń, Marcelina and Żekanowski, Cezary and Falk, Anna and Wężyk, Michalina}},
  issn         = {{1942-0900}},
  keywords     = {{Alzheimer Disease/genetics; Animals; DNA Damage; Humans; Neural Stem Cells/metabolism; Oxidative Stress/genetics; Signal Transduction}},
  language     = {{eng}},
  publisher    = {{Hindawi Limited}},
  series       = {{Oxidative Medicine and Cellular Longevity}},
  title        = {{Oxidative DNA Damage Signalling in Neural Stem Cells in Alzheimer's Disease}},
  url          = {{https://lup.lub.lu.se/search/files/101033467/Oxidative_DNA_Damage.pdf}},
  doi          = {{10.1155/2019/2149812}},
  volume       = {{2019}},
  year         = {{2019}},
}