Neuroinflammation in intracerebral haemorrhage: immunotherapies with potential for translation

Abstract

Intracerebral haemorrhage is inadequately controlled by current treatments, requiring new solutions to improve the prognosis. Following the primary injury, a proinflammatory cascade in the perihaematomal region, composed of activated resident microglia and astrocytes and infiltrated leucocytes, propagates neural cell death. The protracted nature of neuroinflammation in intracerebral haemorrhage provides a window of opportunity for therapies to subdue the undesired consequences. In animal models and early clinical trials in intracerebral haemorrhage, several drugs have reduced detrimental neuroinflammation without substantial compromise of the beneficial reparative aspects of an inflammatory response. Potential strategies include controlling excessive harmful neuroinflammation with minocycline, sphingosine-1-phosphate receptor modulators, and statins after a brain haemorrhage. The quick initiation of these drugs, particularly in high systemic doses, could be key to counteracting the evolving secondary injury in people with intracerebral haemorrhage and provides a promising way in which the poor prognosis of intracerebral haemorrhage might one day be counteracted.