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每周注射醋酸格拉替雷(Copaxone)作为干性年龄相关性黄斑变性的一种潜在治疗方法。

Weekly vaccination with Copaxone (glatiramer acetate) as a potential therapy for dry age-related macular degeneration.

作者信息

Landa Gennady, Butovsky Oleg, Shoshani Johai, Schwartz Michal, Pollack Ayala

机构信息

Department of Ophthalmology, Kaplan Medical Center, Rehovot, Israel.

出版信息

Curr Eye Res. 2008 Nov;33(11):1011-3. doi: 10.1080/02713680802484637.

DOI:10.1080/02713680802484637
PMID:19085384
Abstract

PURPOSE

Drusen formation in age-related macular degeneration (AMD) shares some similarities with Alzheimer's disease (AD), which is associated with amyloid deposits. Aggregated beta-amyloid induces microglia to become cytotoxic and block neurogenesis. Recent evidence showed that T cell-based vaccination with Copaxone in AD mice model resulted in modulation of microglia into neuroprotective phenotype and as a result in reduction of cognitive decline, elimination of plaque formation, and induction of neuronal survival and neurogenesis. The aim was to investigate whether the effect of Copaxone on drusen in dry AMD is similar to that on deposits of other age-related chronic neurodegenerative diseases such as Alzheimer disease (AD).

MATERIALS AND METHODS

Patients over 50 years of age with intermediate dry AMD in both eyes were randomized to receive Copaxone or sham injections and were weekly treated by subcutaneous injections of Copaxone (dose of 20 mg) or sham injections for 12 weeks. At baseline, 6-week, and 12-week visits, visual acuity, contrast sensitivity, fundus examination and photography, fluorescein angiography, and ocular coherent tomography were performed. Main outcome measure was a change in total drusen area (TDA) measured by Image-Pro software and presented in arbitrary units (AU).

RESULTS

Eight studied eyes of four treated patients showed a decrease in TDA from 48130 to 16205 AU at 12 weeks as compared to baseline. In contrast, four control eyes (two patients) demonstrated almost no change in TDA (from 32294 to 32781 AU).

CONCLUSION

These preliminary results show that Copaxone reduces drusen area.

摘要

目的

年龄相关性黄斑变性(AMD)中的玻璃膜疣形成与阿尔茨海默病(AD)有一些相似之处,后者与淀粉样蛋白沉积有关。聚集的β-淀粉样蛋白会诱导小胶质细胞产生细胞毒性并阻碍神经发生。最近的证据表明,在AD小鼠模型中用考帕松进行基于T细胞的疫苗接种可使小胶质细胞转变为神经保护表型,从而减少认知衰退、消除斑块形成并诱导神经元存活和神经发生。目的是研究考帕松对干性AMD中玻璃膜疣的作用是否与对其他年龄相关性慢性神经退行性疾病(如阿尔茨海默病(AD))的沉积物的作用相似。

材料和方法

年龄超过50岁的双眼中度干性AMD患者被随机分为接受考帕松或假注射组,每周皮下注射考帕松(剂量为20mg)或假注射,共12周。在基线、第6周和第12周就诊时,进行视力、对比敏感度、眼底检查和摄影、荧光素血管造影和光学相干断层扫描。主要结局指标是通过Image-Pro软件测量的玻璃膜疣总面积(TDA)的变化,以任意单位(AU)表示。

结果

4例接受治疗患者的8只研究眼在12周时TDA从48130 AU降至16205 AU,与基线相比有所下降。相比之下,4只对照眼(2例患者)的TDA几乎没有变化(从32294 AU降至32781 AU)。

结论

这些初步结果表明考帕松可减少玻璃膜疣面积。

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