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Additionally, the accumulation of senescent glial and neuronal cells has been shown to drive the senescence-associated secretory phenotype (SASP), further amplifying inflammation and oxidative damage

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If our data based on an intense and short exposure to HNE can be extended to an in vivo situation where low concentrations of HNE are produced on a long time scale, the present results suggest that although the amount of DNA adducts is low upon treatment by exogenous HNE, their formation could be favored upon oxidative stress