Healthy neurons, which are postmitotic from birth, are typically paused in the G0 phase of the cell cycle. Senescent neurons feature a senescence-associated secretory-phenotype (SASP), consisting of inflammatory cytokines and chemokines. They also display DNA damage, decayed nuclear envelopes, and organelle damage, including mitochondria and lysosome degradation. Ge et al. performed patch-seq on neurons from individuals with drug-resistant epilepsy, characterizing neuronal morphological, electrophysiological, and transcriptional profiles. This strategy enriched a subpopulation of pathological cortical pyramidal neurons possessing a senescent phenotype. Neurons with this phenotype expressed markers of cell senescence, including β-galactosidase. They also showed increased expression of cell cycle inhibitors (e.g. P21, P53) typically associated with cell cycle arrest. Notably, a mouse model of chronic epilepsy also induced senescent neurons.