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Editors Selection IGR 10-1

Basic research: Optic nerve head: Optic nerve crush

Franz Grus

Comment by Franz Grus on:

17579 Dominant inheritance of retinal ganglion cell resistance to optic nerve crush in mice, Li Y; Semaan SJ; Schlamp CL et al., BMC Neuroscience, 2007; 8: 19


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Glaucomatous optic neuropathy represents a group of neurodegenerative diseases characterized by a progressive death of retinal ganglion cells (RGCs). In addition to risk factors such as elevated intraocular pressure, the family history seems to be of notable relevance. Although in previous studies genetic background in glaucoma were not convincing in most of the studies, Li et al. (495) speculate that all forms of glaucoma have in common that retinal ganglion cells die and this cell death is intrinsic and therefore the susceptibility to optic nerve damage might be influenced by the genes that control this process. Li et al. investigated the susceptibility to optic nerve damage of 15 different inbred lines of mice following optic nerve crush.They found that inbred mice show different levels of resistance to optic nerve crush. Furthermore, they could exclude Bax as a candidate for this process. This study revealed interesting results providing hints for the involvement of genetic backgrounds on the apoptotic processes in retinal ganglion cells. Regarding the analysis of the role of Bax, it would be desirable to investigate the mRNA levels at the site of interest, the eye, instead of the brain, which would provide more useful information. Furthermore, it remains open at which extent these results in mice models can provide at this stage useful information or hints about any genetic involvement to the resistance to optic nerve damage in human glaucoma, because neither none of the mice lines used nor the optic nerve crush are really comparable to the processes in human glaucoma. Furthermore, it remains unclear, if the changes in the susceptibility to optic nerve damage were or have to be caused by genetic variations or by posttranslational modifications of the correlating proteins.



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