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Current ICH therapies, such as surgical evacuation or corticosteroids, often fail to target molecular mechanisms and may exacerbate secondary injury [43]

FASEB J 17:22902292

Yu L, Liu Y, Jin Y, Liu T, Wang W, Lu X, et al

The N-terminal fragment has two immunoglobulin-like domains and binds with high affinity to the major neutrophil chemokine receptors FPR1 and CXCR1, blocking N -formyl-Met-Leu-Phe- and IL-8-induced neutrophil chemotaxis and activation

Future therapies that are neuroprotective and disease-modifying, including novel delivery paradigms by which drugs could be targeted to the CNS to destroy the mutant Huntingtin protein and to arrest disease progression are urgently needed