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Pathophysiology of Late Onset Alzheimers Disease - Research Paper Example

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The paper "Pathophysiology of Late Onset Alzheimers Disease " highlights that Alzheimer’s disease or AD is one of the common diseases seen mainly among old people. It is divided into three major categories; Early-onset AD, Late-onset AD and familial AD…
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Pathophysiology of Late Onset Alzheimers Disease
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? Pathophysiology of "Late Onset" Alzheimer's Disease (LOAD). Alzheimer’s is one of the common diseases seen among old age people everywherein the world. Memory loss is associated with this disease. People considered memory loss as a biological problem in the past; however new scientific studies have shown the close relationship between memory loss and Alzheimer’s disease. Even though Alzheimer’s mostly seen among old age people, modern studies have shown that it can occur even among the people in their forties and fifties. Even though the exact reasons of this disease are still unknown, medical science believes that both environmental and hereditary factors are associated with this disease. Alzheimer’s is normally classified into three different groups; Early onset, Late onset and familial. This paper analyses the dimensions of late onset Alzheimer’s. Pathophysiology of "Late Onset" Alzheimer's Disease It is estimated that more than 4.5 million people in America alone experiencing Alzheimer’s currently. Doraiswamy et al, (2009) have mentioned that Alzheimer’s can occur even at the age of forties or fifties (Doraiswamy et al, 2009, xvii). However, about 90% of the Alzheimer’s disease patients are victims of "Late Onset" Alzheimer's. Alzheimer's victims of more than 65 years of age are normally included in the category of Late Onset" Alzheimer's. Only 10% of Alzheimer's victims are below the age of 65. Normally people below the age of 65 suffers Alzheimer’s because of Down syndrome. This type of Alzheimer’s is known as Early onset Alzheimer’s. On the other hand, "Late Onset" Alzheimer's disease is caused by hereditary and environmental factors. A third type of Alzheimer’s is known as Familial Alzheimer's disease (FAD). In the case of FAD patients, the disease is caused by family history or hereditary. The epidemiology of Alzheimer’s American Academy of Family Physicians (2009) mentioned that Alzheimer's disease starts by changing the recent memory. A person with Alzheimer's disease will remember even small details of his or her distant past but not be able to remember recent events or conversations. Over time, the disease affects all parts of the memory (American Academy of Family Physicians, 2009). The above findings reveal that Alzheimer’s do not have the ability to erase the memory completely. It has the ability to recollect everything in the distant memory while facing problems in recollecting information stored in the recent memory. Bonda et al. (2010) pointed out the imbalances between mitochondrial fission and fusion of cell proliferation as the reason for Alzheimer’s. “Specifically, the dynamic balance of fission and fusion in AD is greatly shifted toward fission, and, as a result, affected neurons contain abnormal mitochondria that are unable to meet the metabolic demands of the cell”(p.181). It should be noted that fission is the process of breaking of cells whereas fusion is the process of combining cells. Both fission and fusion are necessary body mechanisms to maintain good memory. However, in the case of patients with Alzheimer’s fission mechanism occurs more while fusion mechanism occurs less. As a result of that cell proliferation procedures will be troubled and the communication though neurons become defective. It should be noted that neurons are responsible for sending instructions from the brain to different parts of body. This communication process may become defective because of the imbalances in fusion and fission. Risk Factors Advanced age is the primary risk factor for AD; risk doubles every 5 years after the age of 65. Additional risk factors include having a first-degree relative with AD; Down syndrome; head trauma; certain environmental exposures, including metals, infection, and toxins; decreased estrogen levels; and mutations in the APP, PSEN1, PSEN2, or APOE genes. Cardiovascular disease, cardiovascular risk factors (e.g., hypertension, obesity, dyslipidemia, insulin resistance), depression, and certain lifestyle choices (e.g., smoking, lack of exercise, poor diet, and alcohol consumption) can contribute to the development of AD (Buckley, 2012, p.1). There are primary and secondary risk factors associated with AD. Age is the first and most important primary risk factor associated with AD. Age is directly proportional to AD. In other words, as a person getting old, the chances of AD getting increased. Head trauma is another risk factor associated with AD. People who suffered serious brain injuries in the past may develop AD later in their life. It is believed that certain environmental factors also causes AD. It should be noted that we are living in a toxic environment at present. Land, air and water are polluted immensely and as a result of that it is difficult for us to lead a healthy life, The things which we eat, drink, and breath contains toxic elements which can cause AD. According to Fratiglioni et al (1993), “The main risk factor for late-onset Alzheimer’s disease is a family history of dementia, alcohol abuse and occupational exposure”(p.258). These findings clearly establishes the association of hereditary with Late onset Alzheimer’s. it should be noted that dementia is a disease which results in memory loss. Majority of the Alzheimer’s patients are suffering from memory loss. Earlier, people thought that memory loss is a biological process which haunts all old age people. “Twenty years ago people thought that it would be normal for the old people to loss memory because of aging whereas the current studies shown that it was a misconception even though shrinkage of brains cells and the subsequent slower learning of new things may happen” (Fotuhi & Rabins 2004, p.xiv). There are plenty of old age people whose memories are working much better. In some cases, old age people exhibits more memory power than younger people. This anomaly forced scientists to think about the baseless claim of association between age and memory loss. Thus, they started to study this topic more and established the fact that memory loss during old is caused by some kind of disease rather than any biological processes. It is a fact that aging can change the way of storing information in the brain; however, rapid memory loss will never take place because of the anomalies in the storing of information in the brain. Scientific studies proved beyond doubt that long term memories will never be affected by the anomalies in the physiological processes such as storing of information in brain. However, these processes can affect the storing of information in the recent memories or short term memories. Alcoholism and manual work are believed to be the major contributors of Late Onset Alzheimer’s disease (LOAD) (Fratiglioni et al, 1993, 258). In other words, binge drinkers and hard workers are extremely vulnerable to LOAD. Even though hard manual work and alcoholism occurs mostly during young age, its consequences may appear in the form of LOAD later in the life of a person. Treatment options Since the exact reasons for AD are still unknown, it is difficult to treat AD. Even though plenty of psychoactive drugs are used for treating AD, none of them yields satisfactory results. Plenty of researches are going on to develop effective drugs for AD. In many respects, the course of developing therapies for AD has resembled the development of cancer drugs. There were initially only symptomatic therapies, but as the molecular basis of cancer was better understood, there was enthusiasm that a magic bullet could cure and prevent all cancers. The future course of drug development for AD may also track cancer drugs, with therapies that have modest effects on the disease process often used sequentially or in combination with symptomatic therapies, without a major development that cures all. As with some cancer therapies, there are likely to be drugs that dramatically alter the course of only some types of dementia rather than being effective for all dementias (Woodward, 2012, p.58) Future Research According to Wilson et al (2011), “memory functions are under strong genetic influence in older persons with and without AD. This suggests that genetic analyses of memory endophenotypes may help to identify genetic variants associated with AD”(p.249). These findings clearly reveal the association of memory with heredity. In other words, people with strong memory power may have children of the same calibre. Since memory loss is a common phenomenon associated with Alzheimer’s, it is important to research more about the association of heredity with Alzheimer’s. “According to the recent data, AD begins 20–30 years before clinical symptoms become apparent” (Maruszak et al. 2011, p.197). Early diagnosis of this disease may help the medical science to treat it more effectively. So, more researches are necessary to identify the symptoms of this disease before it may actually strike a person. There are plenty of old people, who have good recent memory and distant memory. It is necessary to know more about how such people are capable to maintain such good memory while many others struggle to do so. In some cultures, ADS is seen more common than in other cultures. It is necessary to research more about the cultural attributes of dementia and AD. Conclusions Alzheimer’s disease or AD is one of the common diseases seen mainly among old people. It is divided into three major categories; Early onset AD, Late onset AD and familial AD. Late onset AD usually occurs after the age of 65. Age is the primary risk factor associated with AD. The exact reasons for the occurrence of AD are still unknown. As a result of that effective treatment for AD is still unavailable. Further research is necessary to know more and to find out the reasons and treatment options of AD. References 1. American Academy of Family Physicians (2009), Memory Loss With Aging: What's Normal, What's Not, Retrieved on 31 May 2010 from http://familydoctor.org/online/famdocen/home/seniors/common-older/124.html 2. Buckley, L.L. ( 2012). Alzheimer's Disease. Published by Cinahl Information Systems. Copyright©2012 3. Bonda D.J., Wang, X., Perry, G., Smith, M.A and Zhu X. (2010) Mitochondrial Dynamics in Alzheimer's Disease. Drugs Aging 2010; 27 0 ) : 181-192 4. Doraiswamy PM, M.D., Gwyther LP, M.S.W.& Adler T. (2009), The Alzheimer's Action Plan: What You Need to Know--and What You Can Do--about Memory Problems, from Prevention to Early Intervention and Care, Publisher: St. Martin's Griffin; 1 edition (April 28, 2009) 5. Dr. Fratiglioni L., MD,  Ahlbom, A., PhD,  Viitanen, M. PhD & Winblad, B. PhD. (1993). Risk factors for late- onset Alzheimer's disease: A population- based, case-control study. Annals of Neurology. Volume 33, Issue 3, pages 258–266, March 1993 6. Maruszaka,A. Safranowb, K., Branickic, W., Gawe? K., Walerycha,D., Po?spiechc, E., Gabryelewicza, T., Canterd, J.A. Barcikowskaa, M.and Zekanowskia, C. (2011) The Impact of Mitochondrial and Nuclear DNA Variants on Late-Onset Alzheimer’s Disease Risk. Journal of Alzheimer’s Disease 27 (2011) 197–210 DOI 10.3233/JAD-2011-110710 7. Wilson, R. S., Barrald S, Leed J.H., Leurgans, S.E., Foroudi, T.M., Sweetj, R.A. Radfordk, N.G. Birdl, T.D., Mayeuxd R & Bennett D.A. (2011). Heritability of Different Forms of Memory in the Late Onset Alzheimer’s Disease. Family Study Journal of Alzheimer’s Disease 23 (2011) 249–255. DOI 10.3233/JAD-2010-101515 8. Woodward, M.C. (2012). Drug Treatments in Development for Alzheimer’s Disease Journal of Pharmacy Practice and Research Volume 42, No. 1, 2012. Read More
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