Perinatal insult or injury to the brain—from trauma, intrauterine infections, premature birth, hypoxia, or ischemia—often has devastating neurological consequences, such as epilepsy, cerebral palsy, and behavioral and cognitive problems. “The overall thrust of our current research is to understand the vulnerability of the developing brain to common insults and injuries during the pre- or perinatal periods and to discover why the responses are more severe in children than in adults,” says Nancy B. Schwartz, PhD, director of the Joseph P. Kennedy Jr. Intellectual and Developmental Disabilities Research Center.
One area of active investigation centers on the impact of neonatal traumatic injury on glial cell maturation and the effect of a second insult, increased inflammation, for example, on glial cell differentiation and long-term brain damage. Schwartz and other Kennedy Center researchers developed an animal model that combines two modes of perinatal brain injury—acute trauma and remote-site bacterial infection—and analyzed the biochemical and developmental consequences of each, separately and in combination.
The results to date suggest that multiple mechanisms contribute to the severity of the pathology associated with injury to the developing brain, especially the role of common infections or other insults during pregnancy or soon after birth that may exacerbate long-term impairments. Improved understanding of the contributing factors should inform the development of therapies to ameliorate such damage.
In other research, Schwartz and her colleagues are using a genetic model of Batten disease, in which the normal function of the affected protein and the consequences when it is mutated remain poorly understood. One goal is to identify early markers of degeneration, enabling diagnosis before the first symptoms appear, when it’s too late to rectify the course of this rare but lethal disorder. Schwartz also hopes to identify other pathways that may be targets for therapy—in particular, inflammatory responses that may be inciting events or consequences of damaged or dying cells, with the aim of slowing neurodegeneration via anti-inflammatory treatment.