Purpose To decribe the prevalence of age related macular degeneration (AMD) in the population aged 50 and over in Doumen County of Gunagdong Province. Methods After randomized clustering sampling,all selected individuals were enumerated according to village residence register.Visual acuity were measured by illuminated EDTRS chart. The examination of eyelid,cornea,lens and fundus were also carried out.The diagnosis of AMD was made according to the criteria of National Academic Group of Fundus Diseases combining with the visual criteria of Framingham Eye Study. Results 5 324 indivduals were axamined with participating rate of 92.8%.The ove rall prevalence of AMD was 8.4%.The prevalence of 2.9%,7.8% and 12.9% was found in the age groups of 50-,60-,70- respectively.The prevalence of male and female was 8.5% and 8.4% respctively.5% of AMD eyes were blind and 49% were low vision. Conclusion The prevalence of AMD is hight and increased with aging,but not correlated with sex.AMD can cause severe visual impairment. (Chin J Ocul Fundus Dis,1998,14:122-124)
Objective To observe the characteristics of indocyanine green angiography in exudative age-related macular degeneration. Methods Thirty one cases(36 eyes)were diagnosed as exudative age-related macular degeneration by ocular examination,fundus color photography,fundus fluorescein angiography(FFA)and indocyanine green angiography(ICGA).Their ages ranged from 50 to 82 years.The visual acuities were FC/30cm before eye to 0.7.We analyzed and compared the characteristics of ICGA and FFA in these patients. Results Of 26 eyes with occult choroidal neovascularization(CNV)by FFA,15(57.7%)had classic CNV.Of 4 eyes with serous retinal pigment epithelial detachment(PED)without CNV by FFA,l had serous PED with classic CNV.The hyperfluorescence of the scar stain was defected by ICGA. Conclusion ICGA adds clinically useful information and is important in laser treatment of patients with occult CNV in AMD. (Chin J Ocul Fundus Dis,1998,14:76-80)
According to the best corrected visual acuity and the morphological changes of the macular fovea, responses to the neovascular age-related macular degeneration (nAMD) who receive anti-vascular endothelial growth factor (VEGF) therapy show large variability, including poor and non-responders. Various factors will be reviewed to account for poor and non-response to anti-VEGF therapy, such as the related susceptibility genes, factors related with the development of choroidal neovascularization and morphologic parameters, pharmacokinetics and tachyphylaxis. The future research should focus on comprehensive assessment of factors affecting the efficacy of anti-VEGF therapy to improve the therapeutic outcome of nAMD.
Vascular endothelial growth factor (VEGF) is a multifunctional factor that promotes blood vessel formation and increases vascular permeability. Its abnormal elevation plays a key role in common retinal diseases such as wet age-related macular degeneration and diabetic macular edema. Anti-VEGF therapy can inhibit angiogenesis, reduce vascular leakage and edema, thereby delaying disease progression and stabilizing or improving vision. Currently, the clinical application of anti-VEGF drugs has achieved satisfactory therapeutic effects, but there are also issues such as high injection frequency, heavy economy burden, potential systemic side effects, and non-responsiveness. To address these issues, current research and development mainly aim on biosimilars, multi-target drugs, drug delivery systems, oral anti-VEGF drugs, and gene therapy. Some drugs have shown great potential and are expected to turn over a new leaf for anti-VEGF treatment in ophthalmology.
Lipid globules in retina and choroid are new definitions based on pathology and high-resolution optical coherence tomography (OCT). OCT examination shows that the lipid globules are low reflective circular cavities in the choroid and retina, without strong reflective boundaries around them, followed by a characteristic superreflective tail. It occurs in healthy human eyes and in age-related macular degeneration characterized by retinal pigment epithelium (RPE) atrophy. Its characteristic superreflective tail is the key to distinguishing it from other diseases. At present, the understanding of lipid globules is still in the initial stage. Although lipid globules can be observed in healthy human eyes, a certain prevalence rate indicates that they are associated with choroidal hypoperfusion and RPE atrophy. In the future, larger randomized controlled trials and longer follow-up time are needed to explore its pathogenesis, pathological characteristics and treatment prognosis.
Age-related macular degeneration (AMD) is one of the leading irreversible causes of blindness in China. The pathogenesis of AMD is not fully understood at present. Under various stress conditions, cellular senescence is activated, characterized by telomere shortening, mitochondrial dysfunction, DNA damage, and the release of various senescence-related secretory phenotype factors. Senescence is implicated in the pathogenesis of AMD through multiple pathways, contributing to chronic inflammation and the onset and progression of AMD. Mechanisms such as oxidative stress, lipofuscin, β amyloid protein and the membrane attack complex have become hotspots of study in the pathogenesis of AMD. The cyclic guanosine phosphate - adenosine synthase - interferon stimulating factor synthase-stimulator of interferon gene pathway has emerged as a critical signaling pathway in the early development of AMD, providing direction for further research on AMD. Currently, senolytics, selective agents targeting the induction of senescent cell apoptosis, show significant potential in the treatment of AMD. The integration of new technologies with cellular senescence may offer a novel approach to AMD treatment, and intervening in the AMD treatment through anti-cellular senescence pathways holds promising prospects.
The severe visual impairment caused by neovascular age-related macular degeneration (nAMD) is associated with macular neovascularization (MNV) invasion and subretinal fibrosis (SF). Excessive SF can lead to subretinal scarring, irreversible damage to photoreceptors, retinal pigment epithelium, and choroid tissue, resulting in permanent visual impairment in nAMD patients. The pathogenesis of SF is complex, involving many pathological processes such as tissue repair after injury, inflammation, and related signaling pathways and cytokine complex. Current experimental treatments for SF only target inhibition of a single cytokine. Timely and effective inhibition of the formation and progression of MNV and early identification of risk factors for SF are crucial to improving the prognosis of nAMD patients.
With the tremendous progress in fundus imaging and histopathology over the past decade, the understanding of age-related macular degeneration (AMD) has taken a qualitative leap. AMD is defined as a progressive neurodegenerative disease of photoreceptors and retinal pigment epithelium (RPE) characterized by extracellular deposits under RPE and the retina, including drusen, basal laminar and linear deposits, and subretinal drusenoid deposits, that can evolve to atrophy of the retina, RPE and choroid and neovascularization in the choroid and/or retina. It is the leading cause of blindness and visual impairment in older populations, despite recent advances in treatments. AMD is a multifactorial disease with genetic and environmental factors including advanced age, smoking, high-fat diet, and cardiovascular disorder to enhance the disease susceptibility. The physiopathologic mechanism includes inflammatory processes (complement pathway dysregulation, inflammasome activation), intrinsic (e.g., photo-oxidation) and extrinsic oxidative insult to the retina, age-related metabolic impairment (mitochondrial, autophagic and endoplasmic reticulum stress). Autophagy dysfunction and local inflammation in aged RPE specially result in the extracellular deposits, cell death and AMD. Further investigation of the pathogenesis of AMD will provide with new therapeutic targets and strategy for prevention and treatment of the disease in the early stages.