====== Visual impairment ======

see [[Vision loss]].

see [[Visual field defect]].
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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.))