Researchers at the University of California at San Francisco performed a population-based case-control study of births at Kaiser Permanente Northern California to explore the effect of genetic polymorphisms on the risk of perinatal arterial ischemic stroke (PAIS). Among 13 white infants with PAIS, polymorphisms were genotyped in 9 genes involved in inflammation, thrombosis, or lipid metabolism previously linked with stroke. The apolipoprotein Ee4 allele was associated with an increased risk of PAIS whereas proinflammatory and prothrombotic polymorphisms were not associated with PAIS. [1]

COMMENT. Apolipoprotein Ee4 allele is associated with an increased risk of PAIS in this study and is also linked to cerebral palsy in previous studies [2]. PAIS is a common cause of hemiplegic cerebral palsy. [3]

Genetic deletion of CD36 enhances injury after acute neonatal stroke, in a further study at UCSF [4]. Postnatal day 9 mice were subjected to a transient middle cerebral artery occlusion, and genetic deletion of the scavenger receptor CD36 exacerbates injury after acute focal stroke. Lack of CD36 reduces removal of apoptotic cells, enhancing injury. The injury mechanisms of neonatal stroke and those of adult stroke are compared and contrasted.