Alzheimer's Research Paper

Abstract

The current research revealed a correlation between the presence of the Apo E4 gene and Alzheimer’s disease. Researchers at the Gladstone Institute of Neurological Disease (2004), found that Apo E4 produced by neurons in parts of the brain vulnerable to Alzheimer’s are susceptible to fragmentation. These fragments then lead to abnormal attachments of phosphate groups to brain cells which contort the shape. This finding suggested there may be something in these neurons that when coupled with Apo E4 resulted in the development of Alzheimer’s. If this is the true cause of Alzheimer’s, perhaps inhibiting drugs may be developed to prevent fragmentation of Apo E4. Future studies are needed to determine why fragmentation occurs, why it occurs in some areas and not others, if fragmentation is preventable and whether or not Alzheimer’s will develop if fragmentation is prevented.

Literature Review

Greer (2002), describes the usefulness of genetic testing for families affected by Alzheimer’s. He states that although the presence of the APO E4 gene is correlated with the risk of Alzheimer’s there is no certainty the people with the gene will develop Alzheimer’s. There is a smaller number of people with two copies of the APO E4 gene that live to be over 100 years of age and never develop Alzheimer’s. The current research is not supported by this study, but it does mention a correlation between the presence of the APO E4 gene and the risk of Alzheimer’s disease.

The American Federation for Aging Research (2003), gives a variety of causes leading to a greater risk of Alzheimer’s disease. The relationship between genes and heredity and intellect with the risk of Alzheimer’s is discussed. The article briefly mentions that inheritance of the APO E4 gene increases the risk of Alzheimer’s while inheritance of the APO E2 gene reduces risk. The AFAR cited a study of 100 nuns in Wisconsin over the age of 75. The research reviewed autobiographies written by the nuns over six decades earlier. The nuns whose writing contains less complexity and simpler grammar were more likely to develop Alzheimer’s than those whose autobiographies suggested greater intelligence. This article supports the hypothesis by showing the presence of APO E4 and intellectual ability play a role in the risk and development of Alzheimer’s.

Aldridge (2005), reported that the presence of the APO E4 gene predisposes people to forgetfulness even if they don’t have dementia. A study of prospective memory, cited by Aldridge, on a group of 32 people split into two groups where people were asked to write down a specific word when exposed to a target word was done. Those with the APO E4 gene did significantly worse. It is not clear if those in the APO E4 group were in an early stage of dementia. This article supports the hypothesis by showing the relationship between the presence of the APO E4 gene and memory loss which is associated Alzheimer’s.

The news agency Reuters (2000), reported that the brains of those destined to have Alzheimer’s must work harder to perform various tasks long before any symptoms of Alzheimer’s occur. In a study of 30 volunteers ages 47 through 82 Bookheimer found people with APO E4 utilizea larger part of their brain than those with APO E2, the gene not associated with Alzheimer’s. When retested two years later volunteers who had trouble processing information tended to have poorer memories. This supports the hypothesis by showing the relationship of the APO E4 gene and less efficient functioning of the brain.

Henahan (1998), discussed the discovery of another susceptibility gene. He cited a study by the University of Pittsburgh of the bleomycin gene in 357 Alzheimer’s disease patients and 320 controls. Bleomycin has two forms, A and G. Patients without APO E4 and with two copies of the G bleomycin hydrolase are four times more likely to have Alzheimer’s. This article does not directly support the hypothesis but shows the relationship between Alzheimer’s and specific genes.

The University of Pittsburgh Medical Center links the risk of late onset Alzheimer’s disease with alpha 1-antichymotrypsin or ACT. Investigators studied 225 Alzheimer’s patients 109 of whom were confirmed to have Alzheimer’s through autopsy and 116 of whom were clinically assessed. A control group was used of 315 people without Alzheimer’s ages 42 through 92. There are two forms of ACT. Kamboh, states the first form of the gene increases the risk of Alzheimer’s. He says the risk of Alzheimer’s is dramatically increased when APO E4 is also present.

The UPMC described ACT as a protein that binds to amyloid in the brain and increases in the blood of Alzheimer’s patients. The ACT gene comes in two forms, ACT A and ACT T. The article states that people with ACT A are I.5 times more likely to develop Alzheimer’s disease. Double copies of ACT A and APO E4 increase chances for Alzheimer’s disease by 34 times.

In contrast, people with double copies of APO E4 and ACT T have less of a risk of Alzheimer’s. The article states that people with on copy of the APO E4 gene which by itself increase the risk of Alzheimer’s by 3.5 times but also had double copies of ACT T only had a risk of 3.1 instead. People with double copies of APO E4 and double copies of ACT T had a risk of only 4.4 times greater than average instead of eleven. This article supports the hypothesis by showing that Alzheimer’s results from a combination of genetic risk factors including the presence of the APO E4 gene.

Weng (1994), revealed that discovery of the correlation between the APO E4 gene and Alzheimer’s. She says the cause of Alzheimer’s disease was once thought to be found in the Beta amyloid. The Beta amyloid is a sticky protein that forms insoluble filaments around blood vessels and creates centers of senile plaques in the brains of people with Alzheimer’s disease. Roses, knew that during Alzheimer’s, APO E attaches to the Beta amyloid and accumulate and cause amyloid fibers and plaques to form. This lead Roses to believe

that APO E serves to propagate the disease by controlling if and when the Beta amyloid will form plaques.

Strittmatter (1993), found that APO E attaches itself tightly to Beta amyloid. He then found that APO E is involved with the formation of plaques cholesterol plaques in arteries which can be compared to