Research in neurotrauma and neurodegeneration has highlighted the complex interplay between traumatic brain injury (TBI) and neurodegenerative diseases such as Alzheimer's disease (AD). One study demonstrated that TBI induces tau acetylation, a modification also observed in AD brains, through mechanisms involving S-nitrosylated-GAPDH, which inhibits Sirtuin1 and activates p300/CBP acetyltransferase, leading to increased neuronal ac-tau levels (ref: Shin doi.org/10.1016/j.cell.2021.03.032/). Another significant contribution to this theme is the pooled analysis of strategic infarct locations for post-stroke cognitive impairment (PSCI), which identified a location impact score based on voxel-wise coefficients that effectively predicts PSCI risk, outperforming traditional models that include multiple clinical predictors (ref: Weaver doi.org/10.1016/S1474-4422(21)00060-0/). Additionally, longitudinal transcriptomic profiling in patients with intracerebral hemorrhage revealed dynamic myeloid activation stages, providing insights into the inflammatory responses following brain injury (ref: Askenase doi.org/10.1126/sciimmunol.abd6279/). These findings collectively underscore the importance of understanding the molecular and cellular responses to neurotrauma as potential therapeutic targets for neurodegenerative diseases.