AI Article Synopsis
- Glaucoma is a chronic condition causing optic nerve degeneration, leading to significant vision loss, particularly in older adults.
- Retinal ganglion cells (RGCs) undergo programmed cell death, or apoptosis, primarily through the activation of proteases called caspases, which are also involved in neurodegenerative diseases like Alzheimer's.
- Research suggests that chronic amyloid-beta toxicity might drive RGC death in glaucoma, similar to Alzheimer's, indicating that treatments for one condition could be applied to the other.
Article Abstract
Glaucoma is a chronic neurodegeneration of the optic nerve and one of the leading causes of vision loss in the world among the aging. Retinal ganglion cells (RGCs) have been shown to die by apoptosis, or programmed cell death. Central to apoptosis is the activation of specific proteases, termed caspases. Caspases are activated in chronic neurodegenerations such as Alzheimer's disease (AD) as well as in RGCs after optic nerve transection. In rat glaucoma models we have shown that caspase-3, a major effector of the apoptotic cascade, is activated in RGCs and cleaves amyloid precursor protein (APP) to produce neurotoxic fragments that include amyloid-beta. Caspase-8, which initiates apoptosis after activation of receptors of the tumor necrosis factor (TNF) superfamily, is also activated in RGCs. This suggests a new hypothesis for RGC death in glaucoma involving chronic amyloid-beta neurotoxicity, mimicking AD at the molecular level. With loss of the protective effect of APP and upregulation of toxic APP fragments, RGCs die from chronic caspase activation, loss of synaptic homeostasis, amyloid-beta cytotoxicity and excitotoxicity. The benefits are that treatments for AD could be used to treat glaucoma, and strategies developed to treat glaucoma could treat other neurodegenerations.
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| http://dx.doi.org/10.2741/1172 | DOI Listing |
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