RP is an inherited condition involving more than 50 genes. A genetic disorder that causes retinal degeneration, with no known cure. An estimated 2.4 million people suffer from RP worldwide.
May cause tunnel vision, night blindness .
Currently, there is no cure for RP. Existing treatments to slow the progression of the disease or help with quality of life are restricted in scope.
One gene therapy (RPE65) for a serious form of the condition has been FDA-approved, but it only accounts for around 1% of cases.
Blind patients could use a retinal implant that uses electrical stimulation to transmit signals and provide limited “artificial vision”.
OAG is caused by the slow clogging of the drainage canals for the fluid inside the eye. This gradually increases internal eye pressure (IOP), damaging the optic nerve. At a late stage, the patient manifests symptoms of vision loss, followed by blindness.
OAG is the third leading cause of blindness in the world.
Gradual loss of periphery vision
There are various methods of managing IOP can slow the progression of optic nerve damage. A patient is first prescribed suitable eyedrops; if these are not effective, then an ophthalmologist may consider oral medication or surgical procedures.
Unfortunately, there is no way to revert existing damage to the optic nerve or completely halt progression of the disease, hence 10% of patients that receive current state-of-the-art treatment still go blind.
Anterior ischemic optic neuropathy
There are two types of AION:
Arteritic AION (AAION) is caused by inflammation in the arteries supplying the optic nerve as a result of giant cell arteritis (GCA), killing off nerve cells as a result of insufficient blood supply. AAION causes sudden vision loss in one eye, and if untreated, can blind the other eye as fast as a week later.
Non-arteritic AION (NAION) is a stroke of the optic nerve due to insufficient blood supply, which can be caused by a crowded optic disk, and myriad cardiovascular factors. NAION usually presents itself as a sudden blinding upon waking up, with vision typically stabilizing within 3 months.
Temporary blurriness and loss of vision before vision loss becomes permanent
Current treatment revolves around managing the cardiovascular aspect. In AAION, intervention with high dosages of corticosteroids is necessary to prevent further vision loss. In NAION, no treatment has proved effective: the most rigorous trial conducted so far found that surgical intervention was not useful, but instead harmful to patients.
There is currently no method to restore vision after an AION attack, but there are promising avenues to regenerate the optic nerve after cell death, notably electrical stimulation of the optic nerve.
Age-related macular degeneration
The macula is a small region of the retina responsible for central vision. It contains a very high concentration of cone cells, which contribute to sharp color vision when looking straight ahead.
The cause of AMD is unknown, but major risk factors are age (>60 years old) and smoking. The disease first occurs in its “dry” form, developing in conjunction with deposits below the retina, and progressing slowly. Symptoms such as central vision loss only emerge in later stages, but damage is irreversible.
In 10-20% of cases, dry AMD can develop into wet AMD, where abnormal blood vessel growth and leakage damage retinal cells and eventually lead to blindness.
Distorted vision and loss of central vision
In wet AMD, treatment focuses on restricting the development of the abnormal blood vessels. There are several methods available, including drugs (Anti-VEGF), laser photocoagulation, and photodynamic therapy. A large-scale study also found that certain supplements (vitamin C, beta carotene etc.) could reduce the risk of dry AMD developing into wet AMD.
However, for dry AMD (encompassing the vast majority of cases), there is no known method to slow down retinal degeneration.