Show pageBacklinksCite current pageExport to PDFBack to top This page is read only. You can view the source, but not change it. Ask your administrator if you think this is wrong. ====== Visual impairment ====== see [[Vision loss]]. see [[Visual field defect]]. ---- Visual [[impairment]] in [[diabetes]] is a growing [[public health]] concern. Apart from the well-defined [[diabetic retinopathy]], disturbed [[optic nerve]] function, which is dependent on the [[myelin sheath]], has recently been recognized as an early feature of visual impairment in diabetes. However, the underlying cellular mechanisms remain unclear. Using a [[streptozotocin]]-induced diabetic mouse model, Wu et al. observed a [[myelin]] deficiency along with a disturbed composition of [[oligodendroglia]]l lineage cells in the diabetic [[optic nerve]]. They found that new myelin deposition, a continuous process that lasts throughout adulthood, was diminished during [[pathogenesis]]. Genetically dampening newly generated myelin by conditionally deleting [[olig2]] in [[oligodendrocyte]] precursor cells within this short time window extensively delayed the signal transmission of the adult [[optic nerve]]. In addition, [[clemastine]], an antimuscarinic compound that enhances myelination, significantly restored oligodendroglia and promoted the functional recovery of the [[optic nerve]] in diabetic mice. The results point to the role of new [[myelin]] deposition in [[optic neuropathy]] under diabetic insult and provide a promising therapeutic target for restoring [[visual function]] ((Wu H, Chen X, Yu B, Zhang J, Gu X, Liu W, Mei F, Ye J, Xiao L. Deficient deposition of new [[myelin]] impairs adult [[optic nerve]] function in a murine model of diabetes. Glia. 2023 Jan 20. doi: 10.1002/glia.24341. Epub ahead of print. PMID: 36661098.)) visual_impairment.txt Last modified: 2024/06/07 02:50by 127.0.0.1