Identifying factors that regulate directional growth of regenerating RGC axons to their targets will provide invaluable information on developing future therapies to repair degenerated
optic nerve following glaucoma.
Not exact matches
They found that the mice can develop damage to the
optic nerve despite normal pressure in the eye
following KPro surgery and identified TNFa and IL - 1 as inflammatory factors involved in this process, with high levels of TNFa mediating the damage to the
optic nerve.
Researchers from Massachusetts Eye and Ear / Harvard Medical School have identified inflammatory factors that cause
optic neuropathy in the back of the eye
following implantation of a keratoprosthesis (KPro)-- similar to what glaucoma patients experience, without the rise of pressure in the eye — and have shown that blocking one of those factors, tumor necrosis factor alpha (TNFa), successfully halts the development of
optic nerve damage in a mouse model.
Studies have found beta - amyloid in tissue
following traumatic brain injury and as evidence of
optic nerve damage in shaken - baby syndrome.
We observed YFP - labeled processes exiting the induced eye at the
optic nerve head that
followed the expected trajectory of RGC axons to their tectal targets (Figure 4E).
Ultimately, our research will help elucidate factors that prevent proper
optic nerve regeneration and guidance, and to find strategies that promote reconnection of damaged
optic nerves and restore visual functions
following optic nerve damage.
Glaucoma is a common condition in which the fluid pressure inside your pet's eye increases, resulting in damage to the
optic nerve,
followed by loss of vision and blindness.