Chemotherapy-related changes in central nervous system phospholipids and neurocognitive function in childhood acute lymphoblastic leukemia.

Long-term survivors of childhood leukemia are at risk for neurocognitive impairment, although the neurophysiological basis is not well understood. The purpose of this study was to explore associations between changes in cerebrospinal fluid (CSF) phospholipids and neurocognitive function in children undergoing chemotherapy for acute lymphoblastic leukemia. Seventy-six children were followed prospectively from diagnosis.

Differences in CSF phospholipid concentration by traumatic brain injury outcome.

Traumatic brain injury (TBI) is a leading cause of morbidity and mortality. A cascade of events is initiated with TBI that leads to degradation of the membrane lipid bilayer of neurons and neuroglia. The purpose of this study was to (a) describe changes in the cerebrospinal fluid (CSF) phospholipid concentration over time for those who survived and those who died following TBI; and (b) determine whether there were differences in the CSF phospholipid concentration between those who survived and those who died following TBI.

Oxidative stress and neurobehavioral problems in pediatric acute lymphoblastic leukemia patients undergoing chemotherapy.

Neurobehavioral problems after chemotherapy treatment for pediatric acute lymphoblastic leukemia (ALL) have been a recent focus of investigation. This study extended previous research that suggested oxidative stress as a potential mechanism for chemotherapy-induced central nervous system injury by examining early markers of oxidative stress in relation to subsequent neurobehavioral problems. Oxidized and unoxidized components of phosphatidylcholine (PC) were measured in the cerebrospinal fluid of 87 children with ALL at diagnosis, induction, and consolidation.

Cerebrospinal fluid phospholipid changes following traumatic brain injury.

Traumatic brain injury (TBI) is a leading cause of morbidity and mortality, with approximately 1.4 million people suffering a TBI each year. With TBI, a cascade of events is initiated including the activation of phospholipases, which leads to the disruption of the lipid bilayer of the membrane of neurons and neuroglia.

Methotrexate-induced alterations in beta-oxidation correlate with cognitive abilities in children with acute lymphoblastic leukemia.

Treatment advances, including central nervous system (CNS) treatment with methotrexate, have led to significant gains in disease-free survival from childhood acute lymphoblastic leukemia (ALL). However, methotrexate has been associated with neurological problems such as declines in cognitive and academic abilities. The purpose of this study was to investigate methotrexate-induced changes in beta-oxidation in children with ALL receiving methotrexate for CNS treatment.