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Tau promotes oxidative stress-associated cycling neurons in S phase as a pro-survival mechanism : possible implication for Alzheimer's disease

M Denechaud, Sarah Geurs (UGent) , T Comptdaer, S Bégard, A Garcia-Núñez, LA Pechereau, T Bouillet, Y Vermeiren, PP De Deyn, R Perbet, et al.
(2023) PROGRESS IN NEUROBIOLOGY. 223.
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Abstract
Multiple lines of evidence have linked oxidative stress, tau pathology and neuronal cell cycle re-activation to Alzheimer's disease (AD). While a prevailing idea is that oxidative stress-induced neuronal cell cycle reactivation acts as an upstream trigger for pathological tau phosphorylation, others have identified tau as an inducer of cell cycle abnormalities in both mitotic and postmitotic conditions. In addition, nuclear hypophosphorylated tau has been identified as a key player in the DNA damage response to oxidative stress. Whether and to what extent these observations are causally linked remains unclear. Using immunofluorescence, fluorescence-activated nucleus sorting and single-nucleus sequencing, we report an oxidative stress-associated accumulation of nuclear hypophosphorylated tau in a subpopulation of cycling neurons confined in S phase in AD brains, near amyloid plaques. Tau downregulation in murine neurons revealed an essential role for tau to promote cell cycle progression to S phase and prevent apoptosis in response to oxidative stress. Our results suggest that tau holds oxidative stress-associated cycling neurons in S phase to escape cell death. Together, this study proposes a tau-dependent protective effect of neuronal cell cycle reactivation in AD brains and challenges the current view that the neuronal cell cycle is an early mediator of tau pathology.
Keywords
Alzheimer's disease, Tau, Oxidative stress, Cell cycle, S phase, Pro-survival, COPY-NUMBER VARIATION, CELL-CYCLE, SINGLE-CELL, HUMAN BRAIN, PROTEIN, ACTIVATION, EXPRESSION, REENTRY, DEATH, PHOSPHORYLATION

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MLA
Denechaud, M., et al. “Tau Promotes Oxidative Stress-Associated Cycling Neurons in S Phase as a pro-Survival Mechanism : Possible Implication for Alzheimer’s Disease.” PROGRESS IN NEUROBIOLOGY, vol. 223, 2023, doi:10.1016/j.pneurobio.2022.102386.
APA
Denechaud, M., Geurs, S., Comptdaer, T., Bégard, S., Garcia-Núñez, A., Pechereau, L., … Galas, M. (2023). Tau promotes oxidative stress-associated cycling neurons in S phase as a pro-survival mechanism : possible implication for Alzheimer’s disease. PROGRESS IN NEUROBIOLOGY, 223. https://doi.org/10.1016/j.pneurobio.2022.102386
Chicago author-date
Denechaud, M, Sarah Geurs, T Comptdaer, S Bégard, A Garcia-Núñez, LA Pechereau, T Bouillet, et al. 2023. “Tau Promotes Oxidative Stress-Associated Cycling Neurons in S Phase as a pro-Survival Mechanism : Possible Implication for Alzheimer’s Disease.” PROGRESS IN NEUROBIOLOGY 223. https://doi.org/10.1016/j.pneurobio.2022.102386.
Chicago author-date (all authors)
Denechaud, M, Sarah Geurs, T Comptdaer, S Bégard, A Garcia-Núñez, LA Pechereau, T Bouillet, Y Vermeiren, PP De Deyn, R Perbet, V Deramecourt, CA Maurage, M Vanderhaegen, S Vanuytven, B Lefebvre, Elke Bogaert, N Déglon, T Voet, M Colin, L Buée, Bart Dermaut, and MC Galas. 2023. “Tau Promotes Oxidative Stress-Associated Cycling Neurons in S Phase as a pro-Survival Mechanism : Possible Implication for Alzheimer’s Disease.” PROGRESS IN NEUROBIOLOGY 223. doi:10.1016/j.pneurobio.2022.102386.
Vancouver
1.
Denechaud M, Geurs S, Comptdaer T, Bégard S, Garcia-Núñez A, Pechereau L, et al. Tau promotes oxidative stress-associated cycling neurons in S phase as a pro-survival mechanism : possible implication for Alzheimer’s disease. PROGRESS IN NEUROBIOLOGY. 2023;223.
IEEE
[1]
M. Denechaud et al., “Tau promotes oxidative stress-associated cycling neurons in S phase as a pro-survival mechanism : possible implication for Alzheimer’s disease,” PROGRESS IN NEUROBIOLOGY, vol. 223, 2023.
@article{01GXBFVMZ077WM1FG0NWCSF1ZM,
  abstract     = {{Multiple lines of evidence have linked oxidative stress, tau pathology and neuronal cell cycle re-activation to Alzheimer's disease (AD). While a prevailing idea is that oxidative stress-induced neuronal cell cycle reactivation acts as an upstream trigger for pathological tau phosphorylation, others have identified tau as an inducer of cell cycle abnormalities in both mitotic and postmitotic conditions. In addition, nuclear hypophosphorylated tau has been identified as a key player in the DNA damage response to oxidative stress. Whether and to what extent these observations are causally linked remains unclear. Using immunofluorescence, fluorescence-activated nucleus sorting and single-nucleus sequencing, we report an oxidative stress-associated accumulation of nuclear hypophosphorylated tau in a subpopulation of cycling neurons confined in S phase in AD brains, near amyloid plaques. Tau downregulation in murine neurons revealed an essential role for tau to promote cell cycle progression to S phase and prevent apoptosis in response to oxidative stress. Our results suggest that tau holds oxidative stress-associated cycling neurons in S phase to escape cell death. Together, this study proposes a tau-dependent protective effect of neuronal cell cycle reactivation in AD brains and challenges the current view that the neuronal cell cycle is an early mediator of tau pathology.}},
  articleno    = {{102386}},
  author       = {{Denechaud, M and Geurs, Sarah and Comptdaer, T and Bégard, S and Garcia-Núñez, A and Pechereau, LA and Bouillet, T and Vermeiren, Y and De Deyn, PP and Perbet, R and Deramecourt, V and Maurage, CA and Vanderhaegen, M and Vanuytven, S and Lefebvre, B and Bogaert, Elke and Déglon, N and Voet, T and Colin, M and Buée, L and Dermaut, Bart and Galas, MC}},
  issn         = {{0301-0082}},
  journal      = {{PROGRESS IN NEUROBIOLOGY}},
  keywords     = {{Alzheimer's disease,Tau,Oxidative stress,Cell cycle,S phase,Pro-survival,COPY-NUMBER VARIATION,CELL-CYCLE,SINGLE-CELL,HUMAN BRAIN,PROTEIN,ACTIVATION,EXPRESSION,REENTRY,DEATH,PHOSPHORYLATION}},
  language     = {{eng}},
  pages        = {{18}},
  title        = {{Tau promotes oxidative stress-associated cycling neurons in S phase as a pro-survival mechanism : possible implication for Alzheimer's disease}},
  url          = {{http://doi.org/10.1016/j.pneurobio.2022.102386}},
  volume       = {{223}},
  year         = {{2023}},
}
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