Effect of apolipoprotein E genotype on in-hospital mortality following intracerebral haemorrhage

Abstract

The APOEepsilon4 allele in this population may be associated with poor survival following ICH.

Association of Apolipoprotein E Genotype and Cerebral Palsy in Children

“…Carriage of the 4 allele may also affect outcomes after hemorrhagic stroke. 37 These associations may require confirmation in larger studies. 38 Other mechanisms may contribute to the increased neurologic injury in carriers of the 4 allele.…”

Preclinical Models of Intracerebral Hemorrhage: A Translational Perspective

“…The three common human protein isoforms of apoE, designated apoE2, apoE3, and apoE4, are encoded on human chromosome 19, and differ by single amino acid interchanges at residues 112 and 158: E3 (Cys112 Arg158); E4 (Arg112 Arg158); E2 (Cys112 Cys158) [121]. Several clinical studies have implicated the APOE4 polymorphism with increased mortality and poor functional outcome following ICH [4,122]. The availability of targeted replacement APOE animals has allowed for the exploration of these isoform-specific effects in acute injury models [123].…”

“…For instance, large animal models may be useful for addressing questions of cerebral physiology following ICH, whereas transgenic rodent models may be particularly useful in furthering our understanding of the molecular mechanisms associated with post-hemorrhage brain injury. In particular, transgenic rodent models may be helpful in addressing genetic influences on recovery from ICH, such as has been observed with the APOE polymorphism [4]. Each of the model types has its inherent strengths and weaknesses and has the potential to further our understanding of the pathophysiology and treatment of ICH (Table 1).…”

Genetics of Vascular Cognitive Impairment

“…74 On the injury response side, the presence of the e4 allele has been associated with reduced survival in intracerebral hemorrhage. 58,75 Conversely, an increasing dose of the e4 allele has been associated with improved survival in patients after ischemic stroke, even after adjusting for baseline severity of neurological impairment. 76 Although a useful conceptual model, differentiating incidence from injury-response genes may be difficult experimentally.…”