Fig. 10

Graphical abstract summarizing the main findings of this article. In a senescent context that could be triggered by telomere attrition, neurons increase the transcription of classical senescence markers and display a diminished autophagic flux. Those alterations lead to an aberrant and neurotoxic increase in intracellular Aβ levels. Such an increase is later on translated into decreased extracellular Aβ plaque formation in connecting brain regions