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- W1964696564 abstract "Individuals with neurofibromatosis type 1 (NF1) are prone to developoptic pathway gliomas that can result in significant visual impairment. To explore the cellular basis for the reduced visual functionresulting from optic glioma formation, we used a genetically engineered mouse model of Nf1 optic glioma (Nf1+/−GFAPCKO mice). We performed multimodal functional and structural analyses both before and after the appearance of macroscopic tumors. At 6weeks of age, before obvious glioma formation, Nf1+/−GFAPCKO mice had decreased visual-evoked potential amplitudes and increased optic nerve axon calibers. By 3 months of age, Nf1+/−GFAPCKO mice exhibited pronounced optic nerve axonopathy and apoptosis ofneurons in the retinal ganglion cell layer. Magnetic resonance diffusion tensor imaging showed a progressive increase in radial diffusivity between 6 weeks and 6 months of age in the optic nerve proximal to the tumor indicating ongoing deterioration of axons. These data suggest that optic glioma formation results in early axonaldisorganization and damage, which culminates in retinal ganglion cell death. Collectively, this study shows that Nf1+/−GFAPCKO mice can provide a useful model for defining mechanisms of visual abnormalities in children with NF1 and lay the foundations for future interventional studies aimed at reducing visual loss." @default.
- W1964696564 created "2016-06-24" @default.
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- W1964696564 date "2009-05-01" @default.
- W1964696564 modified "2023-10-18" @default.
- W1964696564 title "Optic Nerve Dysfunction in a Mouse Model of Neurofibromatosis-1 Optic Glioma" @default.
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- W1964696564 doi "https://doi.org/10.1097/nen.0b013e3181a3240b" @default.
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