Abstract: Subarachnoid hemorrhage (SAH) is a severe cerebrovascular disease accounting for a significant portion of young patients with stroke with high morbidity and mortality (van Gijn et al., 2007). Secondary brain injury resulting from neuroinflammation is considered to be a key pathological process (Zheng and Wong, 2017). Microglia, the resident immune cells of the brain, are implicated in numerous neurological diseases, such as Alzheimer’s disease, amyotrophic lateral sclerosis, stroke, and brain tumors (Colonna and Butovsky, 2017). Recent evidence suggests that microglia-mediated neuroinflammation plays a critical role in injury expansion and brain damage after SAH. In fact, two recent clinical studies have shown evidence of microglia accumulation and activation in the human brain parenchyma and cerebrospinal fluid (CSF) respectively after aneurysmal SAH. Schneider et al. (2015) examined 21 patients that had died within the course of SAH which had not suffered central nervous system (CNS) infection nor from cerebral vasospasm and found that microglia accumulation in human brain autopsy specimens after SAH between days 5 and 15 correlated with mortality rate of patients, and at a microscopic level, microglia accumulation was associated with neuronal apoptosis in a distribution concordant to axonal injury. Coinciding with this cellular inflammatory response, they found signs for axonal injury, displayed by an intraparenchymal accumulation of extracellular amyloid precursor protein; they also identified a significantly higher activity of DNA fragmentation in neurons during the course of experiment (Schneider et al., 2015). In cell counts, an increase of neuronal apoptosis could be detected from day 4 onwards to a peak on day 14 after SAH with a corresponding decline in the absolute number of vital neurons (Schneider et al., 2015). Roa et al. (2020) recruited 13 aneurysmal SAH patients for their study and found that the number of CSF microglia cells (CD45dimCD11b+) progressively increased over time after aneurysmal SAH, in particularly in patients with cerebral vasospasm. In contrast, CSF analysis demonstrated elevated counts of natural killer (NK) cells (CD3–CD161+) and Tc17 cells (CD8+CD161+) during the very acute phase on days 0–1, followed by a rapid reduction of cell numbers (Roa et al., 2020). The time course of microglial activation and accumulation suggested a window of opportunity for pharmacological intervention.