Age-related macular degeneration (AMD)
In AMD, this vision becomes increasingly blurred, which means:
reading becomes difficult
colours appear less vibrant
people's faces are difficult to recognise
This sight loss usually happens gradually over time, although it can sometimes be rapid.
AMD doesn't affect your peripheral vision (side vision), which means it will not cause complete blindness.
When to seek medical advice
Why it happens
Dry AMD develops when the cells of the macula become damaged by a build-up of deposits called drusen. It's the most common and least serious type of AMD, accounting for around 9 out of 10 cases.
Vision loss is gradual, occurring over many years. However, an estimated 1 in 10 people with dry AMD go on to develop wet AMD.
Wet AMD – sometimes called neovascular AMD – develops when abnormal blood vessels form underneath the macula and damage its cells.
Wet AMD is more serious than dry AMD. Without treatment, vision can deteriorate within days.
For reasons that are unclear, AMD tends to be more common in women than men. It's also more common in white and Chinese people. The condition is most common in people over the age of 50. It's estimated 1 in every 10 people over 65 have some degree of AMD.
Treating macular degeneration
There's some evidence to suggest a diet rich in leafy green vegetables may slow the progression of dry AMD.
Wet AMD can be treated with anti-vascular endothelial growth factor (anti-VEGF) medication. This aims to stop your vision getting worse by preventing further blood vessels developing.
In some cases, laser surgery can also be used to destroy abnormal blood vessels.
The early diagnosis and treatment of wet AMD is essential for reducing the risk of severe vision loss.
Reducing your risk
Your risk of developing AMD is closely linked to your age and whether you have a family history of the condition. However, you may be able to reduce your risk of developing AMD, or help prevent it getting worse, by:
stopping smoking if you smoke
eating a healthy, balanced diet that includes plenty of fruit and vegetables
moderating your consumption of alcohol
trying to achieve or maintain a healthy weight
wearing UV-absorbing glasses when outside for long periods
Juvenile macular degeneration
Stargardt's disease – the most common cause of juvenile macular degeneration, this can start in childhood or early adulthood
Best's disease – also known as Best's vitelliform macular dystrophy
Sorsby's dystrophy – this often begins between the ages of 30 and 40
Vascular endothelial growth factor (VEGF), originally known as vascular permeability factor (VPF), is a signal protein produced by cells that stimulates vasculogenesis and angiogenesis. It is part of the system that restores the oxygen supply to tissues when blood circulation is inadequate. Serum concentration of VEGF is high in bronchial asthma and diabetes mellitus. VEGF's normal function is to create new blood vessels during embryonic development, new blood vessels after injury, muscle following exercise, and new vessels (collateral circulation) to bypass blocked vessels.
When VEGF is overexpressed, it can contribute to disease. Solid cancers cannot grow beyond a limited size without an adequate blood supply; cancers that can express VEGF are able to grow and metastasize. Overexpression of VEGF can cause vascular disease in the retina of the eye and other parts of the body. Drugs such as bevacizumab and ranibizumab can inhibit VEGF and control or slow those diseases.
VEGF is a sub-family of growth factors, to be specific, the platelet-derived growth factor family of cystine-knot growth factors. They are important signaling proteins involved in both vasculogenesis (the de novo formation of the embryonic circulatory system) and angiogenesis (the growth of blood vessels from pre-existing vasculature).
Anti-VEGF therapies are important in the treatment of certain cancers and in age-related macular degeneration. They can involve monoclonal antibodies such as bevacizumab (Avastin), antibody derivatives such as ranibizumab (Lucentis), or orally-available small molecules that inhibit the tyrosine kinases stimulated by VEGF: lapatinib (Tykerb/Tyverb), sunitinib (Sutent), sorafenib (Nexavar), axitinib, and pazopanib. (Some of these therapies target VEGF receptors rather than the VEGFs.) THC and cannabidiol both inhibit VEGF and slow Glioma growth.
Both antibody-based compounds are commercialized. The first three orally available compounds are commercialized, as well. The latter two (axitinib and pazopanib) are in clinical trials.
Bergers and Hanahan concluded in 2008 that anti-VEGF drugs can show therapeutic efficacy in mouse models of cancer and in an increasing number of human cancers. But, "the benefits are at best transitory and are followed by a restoration of tumour growth and progression."
Later studies into the consequences of VEGF inhibitor use have shown that, although they can reduce the growth of primary tumours, VEGF inhibitors can concomitantly promote invasiveness and metastasis of tumours.
AZ2171 (cediranib), a multi-targeted tyrosine kinase inhibitor has been shown to have anti-edema effects by reducing the permeability and aiding in vascular normalization.
A 2014 Cochrane Systematic Review studied the effectiveness of ranibizumab and pegaptanib, on patients suffering from macular edema caused by central retinal vein occlusion. Participants on both treatment groups showed improvement in visual acuity measures and a reduction in macular edema symptoms over six months.