MD Macular Degeneration

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http://www.gene.com/gene/products/education/vascular/amd.html

Macular degeneration is characterized by a loss of function in the portion of

the eye responsible for central vision. Because central vision makes possible

the detailed sight required to perform daily activities and even recognize

faces, macular degeneration may significantly diminish the ability to function

independently in individuals who suffer from this disease. While some forms of

macular degeneration result from hereditary diseases, most cases occur as part

of the aging process and are known as age-related macular degeneration (AMD).

The Process of Macular Degeneration While the exact cause of AMD is not known,

the disease process begins when the transport of nutrients and waste products

via the retinal pigment epithelial cells (RPE) begins to slow down, leading to

the accumulation of waste products.

Types of AMD There are two forms of AMD: dry (also called non-neovascular) and

wet (neovascular). All cases of AMD begin as the dry form and, for unknown

reasons approximately 10 percent to 20 percent of these cases progress to the

wet form. While both forms ultimately lead to loss of central vision, the

degeneration occurs through different mechanisms and the course of the disease

progression is different.

Dry AMD

Dry AMD tends to progress more slowly than the wet form and is likely to cause

severe loss of central vision or legal blindness in 15 percent to 20 percent of

affected individuals. There are no treatments approved for dry AMD. In dry AMD,

as the waste products build up, retinal cells near the drusen begin to die,

leading to a loss of function in that area of the retina. In some cases, a large

area of cells will die, creating a blind spot in central vision.

Wet AMD

Wet AMD progresses more rapidly, and approximately 90 percent of affected

individuals will advance to loss of central vision and be deemed legally blind.

In wet AMD, the majority of damage to the retina occurs when new blood vessels

begin to grow from the choroid up to the RPE and beneath the retina (a process

known as choroidal neovascularization [CNV] or ocular angiogenesis). While the

exact cause of CNV is unknown, the current hypothesis is that neovascularization

is prompted by the build-up of waste products, diminished function of the RPE,

reduction in oxygen concentration and inflammation. These new blood vessels are

permeable, allowing blood and fluid to leak into the retina. This leakage may

cause the retina to become swollen, impairing function of the retina and leading

to poor or distorted central vision, as depicted below.

http://www.springerlink.com/content/g425rt7j32m5220m/

(CRVO) Central retinal vein occlusion in young people

In a study performed on 20 subjects with central retinal vein occlusion (CRVO)

aged 40 years or less we found the ischemic form in 20%. Disc edema was a common

finding at the onset, while macular edema was less frequently seen. Systemic or

ocular disorders that could be related with the development of the CRVO were

often found; a patient was affected with myasthenia gravis and another with

Sturge-Weber syndrome: these two diseases were not previously reported in

association with CRVO. In only two of the 11 patients followed-up the visual

acuity improved. The visual prognosis in CRVO of young people is often poor; the

more frequent cause of the reduced visual acuity is chronic cystoid macular

edema, ( OK, now I read this last article and makes me wonder if perhaps having

edema in the EYES is a possible cause of this.I think they are not going to know

exactly WHY he has MD so young BUT I do know of other PBCers who also have it.

So.is why I was wonderinf if has to do with having autoimmune disease.and if

this is " just " another DNA marker that is passed down with these genes..........

Curious.anyone elsae know anything on this subject? Joanne