We investigated the role of accelerated senescence on AD neuropathology by crossing telomerase deficient mice (Terc-/-) with mouse models of amyloid and tau pathologies. Our findings suggest that cellular senescence is as an upstream regulator of both amyloid and tau pathologies, positioning it as a critical driver of neurodegeneration and a potential target for therapeutic intervention
Caballol et al. (Wed,) studied this question.