Robert E. Coffee, MD, MPH, Clinical Instructor, Jules Stein Eye Institute, David Geffen School of Medicine, University of California, Los Angeles, USA.
Tara A. Young, MD, PhD, Assistant Professor, Jules Stein Eye Institute, David Geffen School
of Medicine, University of California, Los Angeles, USA.

Age-related macular degeneration (AMD) is the leading cause of blindness among older adults in North America. This article reviews the clinical spectrum, risk factors, pathophysiology, and potential therapeutic options for this disease. Despite significant advances in the treatment of certain forms of AMD, there is currently no cure for this degenerative condition. The substantial personal, social, and economic burden of AMD requires that those who provide care to older adults have a general understanding of this cause of blindness. It is important for the ophthalmologist and primary care physician to address modifiable risk factors for the progression of AMD such as poor cardiovascular status and smoking, which may worsen visual loss. In addition, educating patients and their families regarding risk factors and potential treatment options may greatly benefit those affected by AMD.
Key words: blindness, geriatric, age-related macular degeneration, choroidal neovascularization, ranibizumab, bevacizumab.

Scientists at the Tufts University School of Medicine in Boston have located a protein that may serve as the first molecular marker for the disease glaucoma, and may lead to the development of an early screening test for the disease. Dr. Joel Schuman and colleagues have discovered that the endothelial leukocyte adhesion molecule 1 (ELAM-1), a small cell adhesion molecule that is implicated in the development of vascular diseases, is present in the eyes of patients with glaucoma, but not present in healthy eyes.

The glaucomas, characterized by cupping of the optic nerve head and irreversible loss of retinal ganglion cells, comprise the leading cause of irreversible blindness worldwide. A major risk factor for development of the disease is elevated introcular pressure due to a reduction in normal aqueous outflow. The trabecular meshwork [TM] of the eye forms part of the outflow pathway for aqueous humour as it drains from the back of the eye. If the outflow of the humour is obstructed, the intraocular pressure may rise and glaucoma may occur. ELAM-1 was found to be consistently present on the TM cells in the outflow pathways of eyes with glaucomas of diverse etiology. This study provided the first evidence on a molecular marker for glaucoma, and the first evidence that common mechanisms contribute to the pathophysiology of the glaucomas and vascular diseases. It is believed that abnormalities in the genes encoding ELAM-1 may be considered to be a diagnostic marker of glaucoma, before any damaging rise in intraocular pressure is observed.

Source

1. Wang, N et al. Nature Medicine 2001;7:304-309.