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Biology 202, Spring 2005
Third Web Papers
Alzheimer's disease is an irreversible brain disorder and thus far there is no known cause or cure. It slowly steals the minds of its victims causing memory loss, confusion, impaired judgment, personality changes, disorientation, and loss of language skills. It is a fatal disease, and can be called irreversible dementia.
360,000 cases of Alzheimer's disease are diagnosed each year and by 2050studies show that 14 million Americans will have this disease. Alzheimer's disease is becoming more common every year. Although the cause of Alzheimer's disease is still a mystery, there are two "pathological features that appear in the brains of Alzheimer's victims". These features are amyloid plaques and neurofibrillary tangles. Something typical of Alzheimer's disease is the buildup of amyloid plaques between the neurons in the brain. An amyloid is a term used to describe the protein fragments that are produced by the body naturally. Beta-amyloid is a piece of a protein that is taken from another protein called amyloid precursor protein (APP). (1) In a normal, healthy brain, these fragments of protein would be broken down and removed. However in a brain suffering from Alzheimer's disease, instead the fragments accrue to form solid, insoluble plaques.
Neurofibrillary tangles are insoluble twisted fibers that lie inside the cells in the brain. They consist of a protein called tau, which makes up part of a structure called a microtubule. It aids the body in transporting important substances such as nutrients from one part of the nerve cell to another. Someone suffering from Alzheimer's disease, would not receive this transport as the tau protein is irregular and the microtubule structures subside.
Alzheimer's causes an general reduction of brain tissue. The grooves in the brain, called sulci, are greatly widened and there is a reduction of the gyri, the folds found on the outer layer. The chambers within the brain that hold 'cerebrospinal' fluid, are enlarged. In the early stages, short-term memory begins to decrease which happens when the cells in the 'hippocampus' (part of the limbic system), deteriorate. One is not able to perform routine tasks and as the disease spreads through the cerebral cortex, judgment also declines, along with the ability to speak any language. As the disease progresses more nerve cells die causing behavior changes, such as agitation. The ability to recognize once familiar faces and is totally lost in the final stages along with all type of communication. Patients are not able to control their bowel or bladder, meaning that they need constant care. This state of complete dependency can last for years until the patient dies. Once a patient is diagnosed with the disease, they are expected to live from four to eight years.
There is no known treatment for this disease, however there are many research programs desperately attempting to find some sort of cure for example:
"Alzheimer's Disease Research (ADR), a program of the American Health Assistance Foundation, was established in 1985 to fund research on and educate the public about Alzheimer's disease. Since the program's inception, ADR has awarded more than $43.3 million to support promising research in fields ranging from molecular biology to epidemiology. AHAF is honored to have played a role in Dr. Stanley Prusiner's Nobel Prize in Medicine in 1997 for his landmark research on prions. More than $1.2 million in research grants has been awarded to Dr. Prusiner through its ADR program to develop his prior theory as a model for Alzheimer's disease." (2) .
There are medications currently available for patients to take to help control the symptoms. There are medications that can help control agitation, depression or delusions which are all symptoms that occur with the progression of the disease. Five drugs that are FDA approved can help slow the developement of AD: Cognex, Aricept, Exelon, Reminyl and Namenda. They all slow down the metabolic breakdown of acetylochline(sufferers have a low amount of this chemical), producing more of the brain chemical used for communication between cells. Namenda is used to treat moderate to severe AD, the first drug used in this way. It seems to be able to protect the nerve cells in the brain against large amounts of 'glutamate'. This substance is a chemical released by damaged brain cells in large amounts; they are damaged due to a pathological process that can be associated with AD.
Medications that are used to control depression and anxiety can be used to help patients in the middle stages of AD. Even though they are not designed to help AD they can be part of a treatment plan by doctors. High does of Vitamin E or alpha tocopherol and Selegiline are able to slow the progression of the disease to its most severe. They work by slowing down the loss of brain cells that occurs with the disease. The latter medication actually increases the supply of brain chemicals that diminishes during the disease itself. Selegiline is used on patients suffering from Parkinson's.
Older women taking "combination hormone therapy(estrogen and progestin) had twice the rate of dementia and AD in comparison to those who did not take it. This research was found by Women's Health Initiative (WHI). Researchers decided that combination hormone therapy should not be used on older postmenopausal women for any reason. Estrogen itself is said to increase risk of dementia if it is not taken with progestin.
Other suggested cures have been medications such as Advil or Motrin, easily accessible over the counter medications which can lower the risk of the development of AD or lower the progression rate. Another treatment would be Ginkgo biloba which is made from the leaves of a ginkgo tree. Its properties are :anti inflammatory, anti-oxidant and anti coagulant, it also increases the blood flow to the brain. Some studies have shown it to be beneficial in treating some of the symptoms of AD. The Journal of the American Medical Association said that it was not helpful in helping to treat patients with the disease. It may cause bleeding if combined with aspirin and the long term effects are thus far unknown.
Studies have shown that physical activity appears to slow down Alzheimer's. The research confirmed that long-term physical activity improved the learning capability of mice and diminished the level of "plaque-forming beta-amyloid protein fragments" in their brains.
Therefore lifestyle interventions may help to slow the progression of AD. Scientists are still unaware as to whether physically or cognitively motivating activity might delay the progression of Alzheimer's disease. Scientists have now shown through this study, in an animal model system that a behavioral intervention such as exercise, could delay, or even prevent the development of AD. (3)
There have been interesting studies regarding who develops the disease. Latinos living in the US, with Alzheimer's develop their first symptoms, at a significantly younger age than non Latinos according to a report in the May Archives of Neurology.
"These findings clearly point to the need for extensive, systematic epidemiological studies targeting the U.S. Latino population, our largest and fastest growing minority group, says Maria Carrillo, Ph.D., Alzheimer's Association director, medical and scientific affairs. "The data also suggests that Alzheimer's Disease Centers across the country need to commit time and resources to meet the needs of this population, a huge undertaking but clearly required based on the projected numbers."
A possibility as to why the disease is more common in Latinos is that there is great stress involved in moving to a new country therefore living as an immigrant may make non symptoms associated such as anxiety and depression, both common In people with the illness, more noticeable in Latinos. (4)
In conclusion it seems as though this disease in particular is still waiting for a complete cure. Although many different methods of slowing the disease down have been discovered, scientists are still waiting for a cure that would potentially save over four million Americans.
3) Alzheimer's disease ,
4) Alzheimer's disease
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