Intracerebral hemorrhage in mouse models: therapeutic interventions and functional recovery Balachandar Kathirvelu and S. Thomas Carmichael Department of Neurology, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA Balachandar Kathirvelu: bkathirvelu@ucla.edu Abstract There has been strong pre-clinical research on mechanisms of initial cell death and tissue injury in intracerebral hemorrhage (ICH). This data has led to the evaluation of several therapeutics for neuroprotection or the mitigation of early tissue damage. Most of these studies have been done in the rat. Also, there has been little study of the mechanisms of tissue repair and recovery. This review examines the testing of candidate therapeutics in mouse models of ICH for their effect on tissue protection and repair. This review will help the readers compare it to the extensively researched rat model of ICH and thus enhance work that are pending in mouse model. Keywords ICH; Collagenase; Autologous blood; Functional recovery Introduction Focal stroke is one of the leading causes of death and chronic disability in the United States (Centers for Disease and Prevention 2009; Minino et al. 2011; Go et al. 2013b) and can be broadly classified into ischemic stroke and intracerebral hemorrhage. Ischemic stroke, due to its vast occurrence, has been extensively studied and reported. In the past decade more researchers have started to delve into hemorrhagic stroke, the second common stroke subtype, accounting for 13–15 % of all stroke cases in the United States (Go et al. 2013b). Overall spontaneous brain hemorrhage, based on its location, can be categorized into intracerebral, sub-arachnoid, epidural and subdural (Caplan 2009). Here, we focus only on the intracerebral hemorrhage as it is a subtype of focal stroke and the most common form of brain hemorrhage (Go et al. 2013a). Intracerebral hemorrhage (ICH) occurs due to a breach of a cerebral vessel causing leakage of blood inside the brain parenchyma. Uncontrolled hypertension is a major modifiable risk factor and the leading cause of ICH (Centers for Disease and Prevention 2013; Gillespie et al. 2013; Badjatia and Rosand 2005) with age increasing the incidence progressively © Springer Science+Business Media New York 2014 Correspondence to: Balachandar Kathirvelu, bkathirvelu@ucla.edu. HHS Public Access Author manuscript Metab Brain Dis. Author manuscript; available in PMC 2016 April 01. Published in final edited form as: Metab Brain Dis. 2015 April ; 30(2): 449–459. doi:10.1007/s11011-014-9559-7. Author Manuscript Author Manuscript Author Manuscript Author Manuscript