|Budget Amount *help
¥12,700,000 (Direct Cost : ¥12,700,000)
Fiscal Year 2000 : ¥4,500,000 (Direct Cost : ¥4,500,000)
Fiscal Year 1999 : ¥3,800,000 (Direct Cost : ¥3,800,000)
Fiscal Year 1998 : ¥4,400,000 (Direct Cost : ¥4,400,000)
In glaucomatous eyes, abnormally increased intraocular pressure (IOP) induces retinal ganglion cell death, resulting in loss of visual acuity. At present, most of the drugs and surgeries for glaucoma have been developed for lowering IOPs. Our experimental studies are aimed to protect the cell death of retinal ganglion cells, "neuroprotective therapy, "and repair the damaged axons, "neuroregenerative therapy." In an attempt to rescue retinal ganglion cells from cell death, we investigated the neuroprotective effects of neurotrophic factors in animal glaucomatous models. Our immunohistochemical analyses showed that, in the retinal tissues of animal glaucomatous models, Muller glial cells and astrocytes were activated, and one of neurotrophic factors, ciliary neurotrophic factor (CNTF), was secreted from these glial cells. Moreover, two types of neurotrophic factors, ciliary neurotrophic factor (CNTF) and brain-derived neurotrophic factor (BDNF) showed neuroprotective effects for retinal ganglion cells in animal glaucomatous models. In addition, we demonstrated that two types of chondroitin sulfate proteoglycans (CSPGs), neurocan and phosphacan, were highly expressed in the developing retina. Furthermore, the CSPGs regulated the neurite outgrowth from retinal ganglion cells in vitro, indicating the possibility that the neuroregenerative therapy can be achieved by controlling the expression of the CSPGs. Our investigations will play important roles in developing the new concepts of the treatment for glaucoma.