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Age-related macular degeneration(ARMD)is one of the leading causes of irreversible visual impairment worldwide, and the number of patients is increasing with the aging of the population, with dry ARMD accounting for about 90% of cases. Effective treatments for dry ARMD are currently lacking, making it a prominent area of research. Pharmacotherapy, targeting pathogenic factors such as oxidative damage, inflammation, and vascular issues contributing to ARMD, is one of the main treatments and some drugs have been shown to slow the progression of ARMD. This article reviews drug treatments for dry ARMD, including antioxidant drugs, complement biological agents, non-steroidal anti-inflammatory drugs and immunosuppressants, vasodilators, neurotrophic drugs, as well as traditional Chinese medicine. It summarizes their mechanisms and recent clinical research to contribute valuable insights for the treatment of dry ARMD and the development of novel therapeutic agents.
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@#Age-related macular degeneration(ARMD)is a major cause of irreversible loss of central vision in the elderly. Typical characteristics of ARMD consist of retinal pigment epithelium(RPE), degenerative changes of choroidal capillaries and vitreous warts in macular area. Clinical ARMD is divided into two subtypes: non effusive(dry or atrophic)and effusive(wet or neovascular). The occurrence of the disease is the result of the interaction of many factors, such as age, environment, heredity, smoking, oxidative stress and cardiovascular dysfunction, <i>etc</i>. In view of the important role of RPE cells in pathogenesis of ARMD, the effects and possible mechanisms of blue light, smoking, oxidative stress, lipofuscin accumulation, chronic inflammation and protein homeostasis on the onset of dry ARMD are summarized by focusing on RPE cells. This will provide new ideas to help understand and prevent the occurrence of dry ARMD.
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@#AIM: To explore the differentiation of bone marrow-derived mesenchymal stem cells from peripheral blood to the retina and the expression of ciliary neurotrophic factor(CNTF). We also investigate the mechanism by which Bu Shen Yi Jing Fang could treat dry age-related macular degeneration(ARMD). <p>METHODS:C57BL/6 mice were administered with sodium iodate(NaIO3)by tail intravenous injection. One day after modeling, 3×106 green fluorescent protein labeled bone marrow-derived mesenchymal stem cells(GFP-BMSCs)were injected into the tail vein. The injected mice were randomly divided into distilled water group and Bu Shen Yi Jing Fang group according to random number table, and 12 mice in each group. The mice were intragastrical administrated with either Bu Shen Yi Jing Fang solution or distilled water every day. Twelve healthy C57BL/6 mice were fed regularly as the normal group. At 14d after the treatment, the differentiation of GFP-BMSCs in retina was determined by immunofluorescence, and the expression of CNTF in the retina was detected by immunofluorescence and quantitative real-time PCR.<p>RESULTS: Immunofluorescence staining showed that there were more glial fibrillary acidic protein(GFAP)and GFP double-stained positive cells in the Bu Shen Yi Jing Fang group than in the distilled water group(<i>P</i><0.01), and the positive rate of retinal pigment epithelium 65(RPE65)was not significantly different between two groups(<i>P</i>>0.05). There were no Rhodopsin and GFP double-stained positive cells in the two groups. Immunofluorescence and quantitative real-time PCR showed that the expression of CNTF in the Bu Shen Yi Jing Fang group was higher than which in the distilled water group(<i>P</i><0.05). <p>CONCLUSION: Bu Shen Yi Jing Fang facilitated the differentiation of peripheral blood stem cells into glial cells in the retina and the expression of CNTF, which might be one of the mechanisms of Bu Shen Yi Jing Fang in the treatment of dry ARMD.
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50 years) showed lower MPOD than younger (30–49 years) subjects. But, in the healthy population, the estimated MPOD values exhibited a decreasing trend with age, but there were no significant differences according to age, after excluding patients with AMD. MPOD was significantly lower in patients with AMD than in aged healthy controls. Furthermore, hypertension, dyslipidemia, and smoking were identified as risk factors for AMD.CONCLUSION: MPOD measured with MPSII® reflects the MP density in healthy individuals and patients with dry AMD. Aging was not significantly associated with low MPOD in healthy population, but the presence of dry AMD was significantly associated with low MPOD. Then, low MPOD may be a risk factor for development of dry AMD. Furthermore, routine screening with MPS II® for ages 50 and older is thought to help detect early low MPOD and identify individuals who should take supplements.
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Humans , Aging , Dyslipidemias , Healthy Volunteers , Hypertension , Linear Models , Logistic Models , Macular Degeneration , Macular Pigment , Mass Screening , Methods , Photometry , Retrospective Studies , Risk Factors , Smoke , SmokingABSTRACT
Age-related macular degeneration(AMD) is the major cause of irreversible damage to vision in over 60 years old.Its incidence is increasing with age.Dry AMD is one of the most common types,causing the loss of vision is very slow.At the late stage,the geographic atrophy will be found,in which central vision is severely lost.It is widely believed that chronic inflammantion injury,oxidative stress injury,lipofuscin,drusen and choroid ischemia are the major pathogenesis.Now,the treatment is major aiming to the pathogenesis.But some new therapies such as crocetin,curcumin,ciliary neurotrophic factor,nanoceria,human monoclonal antibody,photoreceptor and stem cell transplantation have some efficiency to dry AMD.This article reviews the research advances in therapy of dry AMD.