Primary and secondary traumatic brain injury (TBI) can cause tissue damage by inducing cell death pathways including apoptosis, necroptosis, and autophagy. However, similar pathways can also lead to senescence. Senescent cells secrete senescence-associated secretory phenotype proteins following persistent DNA damage response signaling, leading to cell disorders. TBI initially activates the cell cycle followed by the subsequent triggering of senescence. This study aims to clarify how the mRNA and protein expression of different markers of cell cycle and senescence are modulated and switched over time after TBI. We performed senescence-associated-β-galactosidase (SA-β-gal) staining, immunohistochemical analysis, and real-time PCR to examine the time-dependent changes in expression levels of proteins and mRNA, related to cell cycle and cellular senescence markers, in the cerebrum during the initial 14 days after TBI using a mouse model of controlled cortical impact (CCI). Within the area adjacent to the cerebral contusion after TBI, the protein and/or mRNA expression levels of cell cycle markers were increased significantly until 4 days after injury and senescence markers were significantly increased at 4, 7, and 14 days after injury. Our findings suggested that TBI initially activated the cell cycle in neurons, astrocytes, and microglia within the area adjacent to the hemicerebrum contusion in TBI, whereas after 4 days, such cells could undergo senescence in a cell-type-dependent manner.

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Summary:The aim of this study was to determine age-related differences in outcome between clipping and coiling in patients with intracranial aneurysms. We retrospectively analyzed 377 consecutive patients (clipping, 304 cases and coiling, 73 cases) dividing them into four groups based on age as follows: <50 years, 50 to 59 years, 60 to 69 years, and ≥70 years. Outcomes were assessed in the perioperative period and 1 year later. Of the cases with perioperative symptomatic events, 7 (2.3%), including 4 cases (1.3%) of symptomatic ischemic stroke, were treated with clipping and none was treated with coiling. All cases of symptomatic perioperative ischemic stroke after clipping occurred in patients aged 60 years (p = 0.027). Events at 1 year occurred only after clipping in 10 cases (3.3%) and after coiling in none of the cases. Eight of 10 patients had chronic subdural hematoma, and all of them were >60 years old (p = 0.028). Favorable outcome was observed for both clipping and coiling in both age groups. Clipping was related to risks of perioperative ischemic stroke and chronic subdural hematoma within 1 year in patients >60 years of age.