Brain damage related to intrathecal methotrexate in children with acute lymphoblastic leukemia (ALL) is still unclear. Neuroinflammatory mechanisms and intracerebral production of specific biomarkers, play a key role in determining neuroprotective mechanisms after brain injury. To determine whether the CSF concentrations of neuron-specific enolase (NSE), neurotrophic factors and doublecortin (DCX) are influenced by repeated intrathecal methotrexate administrations, we prospectively collected CSF samples from 10 children with ALL and 10 controls. Our results showed an increased expression of the liquoral markers. This up-regulation could be interpreted as a neuroprotective response of the brain against the neuronal damages induced by MTX.
Chiaretti, A., Ruggiero, A., Coccia, P., Antonelli, A., Pierri, F., Barone, G., Attina', G., Iuvone, L., Maurizi, P., Riccardi, R., Expression of liquoral neuroprotection markersin children with acute lymphoblastic leukemia, <<LEUKEMIA RESEARCH>>, 2011; 35 (11): 1467-1471. [doi:10.1016/j.leukres.2011.07.025] [http://hdl.handle.net/10807/6706]
Expression of liquoral neuroprotection markers in children with acute lymphoblastic leukemia
Chiaretti, Antonio;Ruggiero, Antonio;Coccia, Paola;Antonelli, Alessia;Pierri, Filomena;Barone, Giovanni;Attina', Giorgio;Iuvone, Laura;Maurizi, Palma;Riccardi, Riccardo
2011
Abstract
Brain damage related to intrathecal methotrexate in children with acute lymphoblastic leukemia (ALL) is still unclear. Neuroinflammatory mechanisms and intracerebral production of specific biomarkers, play a key role in determining neuroprotective mechanisms after brain injury. To determine whether the CSF concentrations of neuron-specific enolase (NSE), neurotrophic factors and doublecortin (DCX) are influenced by repeated intrathecal methotrexate administrations, we prospectively collected CSF samples from 10 children with ALL and 10 controls. Our results showed an increased expression of the liquoral markers. This up-regulation could be interpreted as a neuroprotective response of the brain against the neuronal damages induced by MTX.
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