Glaucom Degenerative Disease

The first disease I’m going to mention is Glaucoma, according to Web MD last updated in 2015, Glaucoma is a condition that causes damage to your eye's optic nerve and gets worse over time. It's often associated with a buildup of pressure inside the eye. Glaucoma tends to be inherited and may not show up until later in life.

A plausible explanation for the thinning of the RNFL in AD is death of retinal ganglion cell axons, and retrograde degeneration due to further loss of cortical neurons. The damage to these cells could be caused by the neurotoxicity of the Aβ aggregates formed during AD. Scientific findings have shown that AD affects the eye, and more specifically produces

The Aβ deposition and diffused plaque formation lead to local microglial activation, cytokine release, reactive astrocytosis and a multi-protein inflammatory response (Eikelenboom

Age-related macular degeneration (AMD) is a common eye condition and a leading cause of vision loss among people age 50 and older. It causes damage to the macula, a small spot near the center of the retina and the part of the eye needed for sharp, central vision, which lets us see objects that are straight ahead.

Age related macular degeneration (AMD) is the leading cause of blindness in people over the age of 50. Every ten years after the age of 50 the prevalence of this disease increases exponentially. Many different factors contribute to the development of AMD including genetic, environment, and metabolic functions. Aside from smoking, abnormal blood pressure, and an unhealthy diet low in fruits and vegetables, many more studies are concluding that similar inflammatory and oxidative processes seen in other age related diseases are also playing a key role in the development of AMD. This disease affects the central areas of the retina and choroid. In return central vision is impaired while peripheral vision is usually not lost. AMD is seen in two different forms, the earlier nonneovascular (dry) type and the more advanced neovascular (wet) type. Each form has its own specific pathology and unique characteristics that set them apart. Fatty, protein deposits called drusens may be the key risk factor in understanding dry AMD pathology, progression, and treatment. Once the more advanced wet AMD is diagnosed, pathology and treatment are targeted around the formation and destruction of abnormal blood vessels, characteristic of the wet AMD eye. The increasing prevalence of AMD has influenced more investigation into what factors can be modulated to prevent the onset or to stop the progression of AMD. This text will discuss the pathology of drusens and the role of inflammation and

Glaucoma is a form of progressive optic neuropathy that has clinically visible structural damage at the ONH and RNFL that correlates to a functional VF deficit1-4. These glaucomatous structural changes include thinning or notching of the NRR, bayonetting of vessels, loss of RNFL,

As humans, we don't always see with our eyes, but often with our imagination (Grunwald, 2016). Often times as people we never realize how useful our vision really is to us. You really don't think about something like that until it would actual happen to you. Throughout this essay, you will learn how the body is affected by Macular Degeneration (MD). Different signs and symptoms, as well as the etiology of MD, will be discussed. In the following, diagnosis tests and treatments may also be listed in order to help others who would like to know more about MD. Not to mention, you will learn the incidence and progression of MD. Furthermore, information though agencies and associations, as well as new research about MD will be given.

Alexander Disease is a rare defect involving the nervous system. It is part of a classification of uncommon genetic disorders called leukodystrophies that affect the central nervous system by interfering with the growth and nourishment of the myelin sheath. Myelin sheath shields nerve fibers and promotes rapid transmission of nerve impulses. If myelin is not properly nurtured, the transmission of nerve impulses can become disrupted causing serious impairment of nervous system functions. Although a majority of cases with early onset exhibit a distinct deficiency in the formation of myelin, white matter defects are sometimes not detected in cases accompanying later onset. Contrary to its classification, the universal characteristic among all Alexander disease cases is actually the presence of atypical protein compounds called Rosenthal fibers. They present themselves in a particular type of glial cell found in the central nervous system known as an astrocyte. Glial cells provide nutrients for neurons, absorb dead neurons, and physically reinforce their structure. Rosenthal fibers are composed of substantial quantities of glial fibrillary acidic proteins (GFAP). GFAP is known to sustain the mechanical strength of astrocytes, but in this case it is a defect in GFAP that has been found to interfere with the function of astrocytes and ultimately causes the leukodystrophy. When tested on mice, the mutation of GFAP caused a new, toxic effect, rather

     Macular Degeneration is a problem in the part of the eye that controls your sharpest central vision. It is a group of diseases that result in a loss of detailed vision. The brain will not just leave the spot empty, so it learns to fill it in with spotty macular cell damage. People most of the time don't tell their doctors (opthalmologists) about it until it is well in advance.

OA is generally recognized as a complex multi-factor disease that has mostly small and modest effect susceptibility loci (Reynard et al., 2012). Over the past decade efforts have been focused on the search for loci that predispose to OA. The following approaches most often have been attempts to provide insight into the complexity of OA genetics: genetic linkage studies (LA), genome-wide association studies (GWAS) and candidate gene studies.

Age related Macular Degeneration or AMD is a disease that affects millions of Americans every year. There are several factors that contribute to this disease, those being: exposure to bright light, diet, hereditary factors and gender. The main ones that can be controlled consist of exposure to bright light and diet. Those that cannot be controlled are hereditary factors and gender. Prevention of macular degeneration consists of reducing the eyes exposure to bright light and the daily diet of the person at risk. What I seek to explore is if adopting to the Mediterranean diet will create the needed health benefit to prevent the onset of AMD. The Mediterranean diet is one which focuses on eating seafood, fruits, vegetables, whole grains, legumes and healthy fats from things such as olive

In 2007 geneticists at National Institute of Aging reports that a genetic risk factor called SORL1 was found in the development of Alzheimer’s (National Institute of Aging, 2008). According to Mattson (2004) mutations in PS1 and PS2 are believed to cause Alzheimer’s by increasing production of the neurotoxin (substance causing damage to nerves) forms of AB (antibody). Along with individuals that inherit E4 isoform (protein) are at increased risk of developing Alzheimer’s.

Glaucoma is a group of eye disorders that cause blindness by hurting the optic nerve, which is the large nerve that is responsible for vision. In glaucoma, the optic nerve damage is related to a change in the fluid pressure that circulates around the eyeball. In many cases, Glaucoma occurs when the eye's fluid pressure is high, but it can also occur when the pressure is measured as normal.

Alzheimer's disease is a degenerative neurological disorder that is now the sixth leading cause to death in the United States. In the recent years several genes have been pinpointed that are responsible for the disorder, along with twenty genes that have been known to increase and decrease the risk of getting it. Although this newly learned information is helpful it does not fully explain the cause. Scientists have been searching relentlessly to find the explanation to onset Alzheimer's.

On any single day, people come across an array of different eye-colors. Some of the most common known eye colors include brown, blue, green, and hazel pigments. But there are plenty of “in-between” colors that are often overlooked. For example, individuals with blue eyes might express light blue pigment in the iris of their eyes, while others might express dark blue pigment. It is interesting how eye-color can change as an individual ages. Some of the questions that will be addressed in this paper include the number of genes involved in the phenotypic expression of this trait, what those genes are, and which chromosome or chromosomes these gene(s) are found on. Often when the phenotypic expression of a trait is continuous, it can be predicted that there is more than one gene involved in coding for the trait. This can be referred to as a polygenic trait.