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Article Dans Une Revue Progress in Neurobiology Année : 2023

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

Sarah Geurs
  • Fonction : Auteur
Bruno Lefebvre

Résumé

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 hypo- phosphorylated tau in a subpopulation of cycling neurons confined in S phase in AD brains, near amyloid pla- ques. 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
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Origine : Publication financée par une institution

Dates et versions

hal-04309994 , version 1 (23-02-2024)

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Marine Denechaud, Sarah Geurs, Thomas Comptdaer, Séverine Bégard, Alejandro Garcia-Núñez, 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, pp.102386. ⟨10.1016/j.pneurobio.2022.102386⟩. ⟨hal-04309994⟩

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