Inflammation in the pathogenesis of age-related macular degeneration
- Atsuhiro Kanda1,
- Goncalo Abecasis2,
- Anand Swaroop1,3,4
- 1Department of Ophthalmology and Visual Sciences, University of Michigan, Ann Arbor, MI, USA
- 2Department of Biostatistics, University of Michigan, Ann Arbor, MI, USA
- 3Department of Human Genetics, University of Michigan, Ann Arbor, MI, USA
- 4Neurobiology, Neurodegeneration & Repair Laboratory, National Eye Institute, National Institutes of Health, Bethesda, MD, USA
- Dr A Swaroop, Neurobiology, Neurodegeneration & Repair Laboratory (N-NRL), National Eye Institute, National Institutes of Health, Bldg 10/10B11, MSC1864, Bethesda, MD 20892, USA; swaroopa{at}nei.nih.gov
- Accepted 6 December 2007
Degenerative diseases of the retina can have a devastating impact on quality of life and constitute a major cause of untreatable blindness in developed countries. Age-related macular degeneration (AMD) stands out among these, as it leads to visual dysfunction in a significant fraction of the elderly population worldwide. AMD primarily affects the macular region of the retina; early signs of the disease include the appearance of soft drusen and regions of altered pigmentation in the retina, whereas advanced stages exhibit choroidal neovascularisation or atrophy of photoreceptors and the retinal pigment epithelium (RPE).1–3 Diverse cellular processes have been implicated in AMD pathogenesis, including inflammation, oxidative stress, altered cholesterol metabolism and/or impaired function of the RPE.3–6 It is widely believed that manifestation of distinct disease characteristics in AMD is the result of a complex interplay among genetic and environmental factors.7 8 Although the casual pathways underlying AMD are not fully understood, this multifactorial neurodegenerative disease has received considerable attention in the last few years, as rapid advances in genetics and genomics have provided insights into the underlying pathophysiology, potentially opening …
