Neurology Volume 72(7) February 17, 2009 by AAN Copyright © 2009 by AAN Enterprises, Inc PDF

By AAN Copyright © 2009 by AAN Enterprises, Inc

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Additional resources for Neurology Volume 72(7) February 17, 2009

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Analysis of mRNA extracted from lymphoblasts in our family showed the mutation was clearly present in the cDNA on sequencing of the proband and the unaffected heterozygous mother; affected mRNA was not degraded at 26, 28, and 30 cycles as would be expected with NMD. These data indicate that a truncated protein may be translated; however, a rapid protein degradation and resulting haploinsufficiency cannot be excluded at this stage of the investigation. 8,9 This may be due to a genotype-phenotype effect although the position and type of the mutation is similar and in close proximity to three other reported stop mutations.

8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 23. 24. Chiaretti A, Genovese O, Riccardi R, et al. Intraventricular nerve growth factor infusion: a possible treatment for neurological deficits following hypoxic-ischemic brain injury in infants. Neurol Res 2005;27:741–746. Collin T, Arvidsson A, Kokaia Z, et al. Quantitative analysis of the generation of different striatal neuronal subtypes in the adult brain following excitotoxic injury. Exp Neurol 2005;195:1–80. Ong J, Plane JM, Parent JM, et al.

Functional interactions of neurotrophins and neurotrophin receptors. Annu Rev Neurosci 1995;18:223–253. 30. Cui Q. Actions of neurotrophic factors and their signaling pathways in neuronal survival and axonal regeneration. Mol Neurobiol 2006;33:155–179. 31. Cheng B, Mattson MP. NT-3 and NGF protect CNS neurons against metabolic/excitotoxic insults. Brain Res 1994; 640:56–67. 32. Holtzman DM, Sheldon RA, Jaffe W, Cheng Y, Ferriero DM. Nerve growth factor protects the neonatal brain against hypoxic-ischemic injury.

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Neurology Volume 72(7) February 17, 2009 by AAN Copyright © 2009 by AAN Enterprises, Inc

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