Alzheimer’s Disease, Research Paper Example
Words: 1048Research Paper
The National Institute on Aging (NIA) defines Alzheimer’s disease as “an irreversible, progressive brain disease that slowly destroys memory and thinking skills.” (nia.com). Research indicates that the disease is most prevalent in individuals over the age of sixty-five. The Alzheimer’s Association estimates that 5.4 million or 1 in 8 Americans 65 and older suffer from the disease. By 2050, that number is expected to grow to over 13 million (alz.org). This paper examines the physiological effects of Alzheimer’s, how the disease progresses, the typical symptoms of the disease and strategies that might be adopted in the treatment of the disease.
Organ System Functions
Alzheimer’s disease attacks the brain and as the disease progresses through the moderate and severe phases, it affects the human physiology in general including the functioning of other organs in the body. Clinical research has demonstrated that Alzheimer’s causes the nerve cells and other tissues in the brain to deteriorate over time, sometimes over a span of twenty years. This deterioration causes significant shrinkage within the brain. Autopsies on patients who die from Alzheimer’s show the diseased brains at half the size of a normal brain and a substantial darkening of color of the cerebral cortex. Alzheimer’s can affect all parts of the brain depending upon the stage of progression (Goedert & Spillantini, 2006, p.778).
Researchers believe that the primary cause of impairment is through the disruption of the brain’s neurotransmitters which control certain critical life functions such as memory and speech. Cross sections of diseased brains consistently show three effects of Alzheimer’s disease; a shrinking of the cortex, significant deterioration in the hippocampus that plays a vital role in controlling memory and a build-up of fluid in the brain’s ventricles that cause the ventricles to be enlarged.
In Alzheimer’s patients, researchers have discovered that the protein surrounding the nerve cells in the brain breaks down forming beta-amyloids and tau triangles. This causes a type of plaque build-up which eventually destroys the brain’s neurons. The effect of this plaque build-up over time can be clearly seen using MRI technology (LaFerla et al, 2007, p. 501).
Risk and Symptoms
Alzheimer’s can be as difficult to diagnose as it is to treat. There is no single cause or a definitive treatment that is known to the medical community. One of the major problems in detecting Alzheimer’s is that the disease often develops slowly over a period of many years. General practitioners are often forced to rely on verbal reports from family members of patients that exhibit the symptoms that are associated with the disease. There is no blood test or other diagnostic tool that can provide guidance to the physician.
The clinical research seems to indicate that onset of Alzheimer’s is a result of a number of risk factors that work in combination to cause the disease. Previous cognitive behavioral issues, prior head trauma, diet, high blood pressure, history of medications and high cholesterol are believed to be related to Alzheimer’s.
There also appears to be a genetic predisposition for the disease. In over fifty percent of Alzheimer’s cases where there is a family history of the disease, researchers have discovered the existence of three defective genes that interrupt the normal activities of specific neurotransmitters in the brain. Defects in the Amyloid Precursor Protein Gene and two genes called Presenilin 1 and Presenilin 2 have been linked to Alzheimer’s disease. In these cases, abnormal levels of protein are produced in the brain (Shaw et al, 2009, pp. 405-407).
The data also indicate that two-thirds of all cases reported in the U.S. are in women over sixty-five years of age, although doctors have yet to determine why the disease affects women at a much higher rate than men. African Americans and Hispanics over sixty-five are twice as likely to develop Alzheimer’s than whites (nia.gov).
A number of symptoms are associated with Alzheimer’s disease. Acute loss of memory is the most common symptom. In the early phase of the disease, Alzheimer’s patients exhibit an inability to solve routine problems. Moreover, they are easily confused in attempting to address routine life issues. As the disease progresses, the patient may go through personality changes, have difficulty speaking and articulating thought processes in verbal communication and they often exhibit an inability to process information provided through visual media.
As noted earlier, there is no cure for Alzheimer’s disease. Most doctors recommend a combination of psychotherapy and pharmaceutical interventions. Family support and care is also a critical component of the treatment plan.
To date, the Food and Drug Administration has approved five drugs specifically for Alzheimer’s treatment. Four of these drugs are cholinesterase inhibitors. They are Reminyl, Cognex, Aricept, and Etelon. These drugs have shown some success in limiting the deterioration of the neurotransmitter, Acetylcholine which affects memory loss. The fifth drug, Namenda, is a N-methyl D-asparate antagonist drug which regulates the production of Glutamate in the brain. Excess levels of Glutamate are known to destroy brain cells (fisher foundation.org).
The most promising area for treatment is in the area of genetic therapy. A major clinical study, sponsored by the National Institutes for Health, is currently underway at twelve medical research centers in the United States. The treatment involves injecting a genetic transfer agent called CERE-10 directly into the brain. This stimulates the production of the protein NGF which has the potential to restore damaged nerve cells in the brain (Nilsson et al, 2010, pp. 742-747).
Alzheimer’s is a debilitating disease and the cost of its treatment continues to grow at an alarming rate. Stem cell research and the use of genetic therapies hold much promise for Alzheimer’s patients and their families. Government organizations and private foundations need to invest additional resources in further research so that a cure can be found.
Alzheimer’s Association website retrieved from http://alz.org.
Fisher Foundation for Alzheimer’s Research website retrieved from http://alzinfo.org.
Goedert, Michel & Spillantini, Maria G. (2006). A century of Alzheimer’s disease. Science, 314(5800), 777-781.
LaFera, Frank M., Green, Kim N., & Salvatore, Oddo. (2007). Intracellular Amyloid-B in Alzheimer’s disease. Nature Reviews Neuroscience, 8, July, 499-509.
National Institute on Aging (NIA) website retrieved from http://www.nia.nih.gov/alzheimers.
Nilsson, Per, Iwata, N., Maramatsu, Shin, Tjernberg, Lars O., Winblau, Bengt & Saido, Takaomi (2010). Gene therapy in Alzheimer’s disease—potential for gene modification. Journal of Cellular and Molecular Medicine, 14(4), 741-757.
Shaw, Leslie M. et al. (2009). Cerebrospinal fluid biomarker signature in Alzheimer’s disease neuroimaging initiative subjects. Annals of Neurology, 65(4), 403-413.
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