Microglial Responses to Intracranial Hemorrhage

Microglial activation has been increasingly recognized as an important mediator of disease processes following intracranial hemorrhage, including subarachnoid hemorrhage from aneurysmal rupture, intraparenchymal hemorrhage in the setting of hypertension, or intraventricular hemorrhage. For instance, in the context of vasospasm, microglial activation may play a crucial role in neuro-inflammation, leading to its initiation. Cognitive decline has been linked to the tagging of synapses with C1Q/C3 and their subsequent elimination by microglia if the complement cascade is activated following increases in intracranial pressure (ICP) in the setting of hemorrhage.

The goal of this Research Topic is to provide a comprehensive review of microglial responses to various types of intracranial hemorrhages and explore the intricate involvement of microglial activation in secondary complications, such as vasospasm, brain edema and cognitive decline.

This collection welcomes manuscripts covering:

- The role of microglial activation in cognitive decline following intracranial hemorrhage

- The role of microglial activation in vasospasm after subarachnoid hemorrhage

- The role of microglial activation in brain edema formation and/or blood-brain barrier function after intracranial hemorrhage

- Links between microglial activation and inflammatory pathways leading to secondary injuries

- Diagnostic tools and biomarkers related to microglial responses

- Therapeutic interventions targeting microglial activation and complement cascade signaling or other downstream neuro-inflammatory pathways in post-hemorrhagic complications

This Research Topic welcomes pre-clinical studies, clinical studies, reviews, and opinion papers. Case reports are not accepted.