Vickers J C
Division of Pathology, Clinical School, University of Tasmania, Hobart, Australia.
Aust N Z J Ophthalmol. 1997 May;25(2):105-9. doi: 10.1111/j.1442-9071.1997.tb01290.x.
Evidence is presented that the characteristic pattern of neuronal degeneration associated with glaucoma is due to a combination of the persistent physical damage to axons at the level of the lamina cribrosa and the associated neuronal reaction to this kind of trauma. The class of neuronal cytoskeletal proteins known as the neurofilament triplet are crucially involved in the reaction to physical damage and the selective localization of these proteins to larger retinal ganglion cells may underlie their susceptibility to eventual degeneration. The appearance of glaucoma-like neuronal pathology in Alzheimer's disease may follow the reaction of neurofilament-containing retinal ganglion neurons to persistent damage to their axons by beta-amyloid plaque formation in subcortical visual centers.
有证据表明,与青光眼相关的神经元变性特征模式是由于筛板水平轴突持续受到物理损伤以及神经元对这种损伤的相关反应共同作用所致。被称为神经丝三联体的神经元细胞骨架蛋白类在对物理损伤的反应中起关键作用,这些蛋白在较大的视网膜神经节细胞中的选择性定位可能是它们最终易发生变性的基础。阿尔茨海默病中青光眼样神经元病理改变的出现可能是由于含神经丝的视网膜神经节神经元对皮质下视觉中枢中β-淀粉样蛋白斑块形成导致其轴突持续损伤的反应。