Abstract: Advanced microsystems in traumatic brain injury research: Traumatic brain injury (TBI) results from a mechanical insult to the brain, leading to neuronal and axonal damage and subsequently causing a secondary injury. Within minutes of TBI, a neuroinflammatory response is triggered, driven by intricate molecular and cellular inflammatory processes. The temporal progression of TBI events has been investigated using animal models, human surgical and post-mortem tissue samples, and the analysis of cerebrospinal fluid and plasma from TBI patients. However, the complex interplay between injured brain cells remains poorly understood. TBI induces immediate cell death at the site of impact (primary injury), which is dependent on the severity and depth of the injury. Damaged cells release damage-associated molecular patterns, which signal to resident and infiltrating immune cells via pattern recognition receptors. At the injury site, astrocytes, microglia, and damaged neurons secrete cytokines and chemokines, which activate microglia and astrocytes, and recruit peripheral immune cells that penetrate the compromised blood–brain barrier during the acute post-traumatic period (Nespoli et al., 2024). Consequently, TBI is a mechanobiological disorder characterized not only by the dysregulation of neuronal cells but also by a complex interplay of signaling pathways among brain cells.