Literature Review on Alzheimer’s disease Essay Example

Literature Review on Alzheimer’s disease Essay Literature Review on Alzheimer’s disease Name Institution Course We will write a custom essay sample on Literature Review on Alzheimer’s disease specifically for you for only $16.38 $13.9/page Order now We will write a custom essay sample on Literature Review on Alzheimer’s disease specifically for you FOR ONLY $16.38 $13.9/page Hire Writer We will write a custom essay sample on Literature Review on Alzheimer’s disease specifically for you FOR ONLY $16.38 $13.9/page Hire Writer Instructor Section # Email Address It is the intent of this review of the literature to show the need for further research in the area of Alzheimer’s disease in order to add to the existing body of knowledge in the area of this disease. The literature review has shown a gap in the literature and the need for further research in the area of Alzheimer’s disease Delavande et al, (2013) delineates dementia as a persistent condition intrinsic of aging that is illustrated by cognitive degeneration. Examples demonstrate the affected losing independence as well as a huddle of indicators brought by this medical condition. Commonly referred to as a disease of aging people, Alzheimer’s disease is the most familiar type of dementia among elder individuals. Dementia is a disease within the brain that austerely affects an individual’s ability to perform routine activities. Burns (2006) asserts that Alzheimer’s disease is a successive neurological brain condition that leads to the permanent depravity of neurons and intellectual capabilities, including reminiscence and logic. Furthermore, dementia, as a medical condition, is exemplified by a huddle of indicators and signs, which are evidenced by memory complexities, language instabilities, psychosomatic and psychiatric deviations, and disabilities in performance of routine tasks. In clinical follow-up, interventions that involve non-usage of drugs should be attempted foremost specifically in the event where symptoms do not lead to distress nor risk the respective individual. It is also fundamental to include therapeutic interventions, which are suited for the victim and create a fair affinity with the individual affected by dementia. Additionally, the use of Cholinesterase inhibitors as a form of medicinal treatment is essential in curing Alzheimer’s disease. This is because the treatment r estricts Cholinesterase, which dissolves acetylcholine, hence increasing the degree of neurotransmitters and leading to altering of the symptom. Ferri et al, (2112) research demonstrates that Alzheimer’s disease is a particular illness that affects nearly 6 percent of the populace aged above 65 and enhances in frequency with age. Consequently, Alzheimer’s disease is identified by three classes of symptoms. The first category is based on cognitive dysfunction. At this point, cognitive dysfunction incorporates symptoms such as complexities in language, loss of cerebral coordination aptitudes and memory. The second category includes psychosomatic indicators and disturbances in behavior, for instance, delusions, depression, agitation and hallucinations, which are solely deemed as non-cognitive signs. The third category incorporates difficulties associated with the performance of routine activities, which are characterized as instrumental based on technical activities that include driving or operating and basic, which comprise tasks such as eating or unassisted dressing. Alzheimer’s disease is a successive neu rological brain condition that leads to the permanent depravity of neurons and intellectual capabilities, including reminiscence and logic, which become ruthless enough to obstruct societal or professional functioning. Ferri et al, (2112) adds that Alzheimer’s disease is a particular illness that affects nearly 6 percent of the populace aged above 65 and enhances in frequency with age. Cooper, Shanks and Venneri, (2006) demonstrates that collectively, signs of Alzheimer’s disease develop from mild symptoms of memory deprivation to severe dementia. Progressively, the mutual existence of disease associated with vessel malfunctions and Alzheimer’s disease is being identified clinically, pathogenically and epidemiologically, because the disease inhibits regular motor skills thereby increasing the risk to contract cardiovascular diseases among aged people who experience progressive stern Alzheimer’s disease. Reitz, Patel and Luchsinger, (2007) uses their research to show that the relation between risks associated with vascular diseases compound the risk of augmenting Alzheimer’s disease among old persons. Various controversies arise that encompass the notion of mild cognitive disability. For instance, one controversy is based on the importance of recognizing mild cognitive disability in order to facilitate preventive involvements. Another controversy is based on normal aging, whereby recognition of mild cognitive disability is deemed as being as a precursor towards medicalization of ordinary aging. Regardless of the controversies, research indicates that individuals possessing mild cognitive disability are more likely to have gained dementia, thus indicating that the dysfunction can actually be considered as an antecedent to Alzheimer’s disease. Matthews et al, (2008), use population studies based on aging and cognition to indicate that disabilities in numerous cognitive areas are identified even before diagnostics on Alzheimer’s disease are performed. Research conducted on the relation between aging and Alzheimer’s disease is crucial to determine the disease’s nature in targeting the aging population. Brayne (2007) shows that experimental cognitive malfunction is not different from that witnessed in ordinary aging, signifying stability rather than discontinuity in the change from regular aging to premedical dementia. Inclusive cognitive decline, which affects memory and other facts of cognitive operation such as attention and perceptual speed, is always an indicating symptom. There is considerable convergence in cognitive functioning between ordinary aging and deterioration in cognition and insignificant proof exists that is yet to identify that these changes are evident or recognizable in medical encounters. (Strozyk et al, 2010) demonstrates that an individual exhibiting signs of Alzheimer’s disease is more likely to show the observable characteristics of dementia if they possess mutual symptoms of vascular ailments. There is considerable convergence in cognitive functioning between ordinary aging and deterioration in cognition and insignificant proof exists that is yet to identify that these changes are evident or recognizable in medical encounters. The focus on treatments for the disease is sharpened by the incorporation of psychosomatic interventions that are proper for treating dementia irrespective of its causes. Typically, a considerable number of psychosomatic interventions and medicinal treatments provide symptomatic advantages and therefore do not rely for their effectiveness on altering the core pathophysiology. For instance, depression treatment within dementia is fundamentally similar regardless of the cause of dementia based on Alzheimer’s disease or dementia in retrospect of vascular features. Nestor, Scheltens and Hodges (2004) utilize rigorous tests of periodic memory that are the preferred neuropsychological forecasters of consequent change from mild cognitive disability to Alzheimer’s disease currently. Longitudinal research on cognitive dysfunctions pertaining to Alzheimer’s disease asserts that cognitive disabilities in the beginning phases are likely to continue being invariable for a number of years. These stages match to the clinical perception of placid cognitive impairment, whereby the person possesses subjective symptoms such as memory loss and quantifiable cognitive insufficiencies but lacks impairment in performing daily activities. Longitudinal research on cognitive dysfunctions pertaining to Alzheimer’s disease asserts that cognitive disabilities in the beginning phases are likely to continue being invariable for a number of years. These stages match to the clinical perception of placid cognitive impairment, whereby the person possesses subjective symptoms such as memory loss and quantifiable cognitive insufficiencies but lacks impairment in performing daily activities. Spaan, Raaijmakers and Jonker, (2003) show that stability in mild cognitive disability leads to cognitive deterioration, whereby semantic memory, which signifies the hoard of particulars and common knowledge, and implicit memory, which refers to influence of experience on current functioning, degrades. Techniques used in brain imaging are able to recognize composite and metabolic changes in the brain. However, there is no technique to identify if individuals possessing mild cognitive disability arte more susceptible to gain Alzheimer’s disease. The inception of Alzheimer’s disease is usually identified by memory loss. Majority of Alzheimer cases depict memory loss as the foremost sign of Alzheimer’s disease among patients. The steady inception of memory loss indicates that it is susceptible towards being identified mistakenly to ordinary aging and is considerably identified specifically as the beginning of Alzheimer’s disease. The inception is subtle, begi nning with mild memory loss and word finding difficulties, which are symptoms that are viewed as regular in daily life. Regardless, an integration of imaging and psychological tests enhances the accuracy of forecasting cognitive deterioration in individuals. Nevertheless, the techniques for recognition of beginning changes characteristic of Alzheimer’s disease are outpacing the curative options such that there is uncertainty based on the efficacy of such premature preclinical diagnoses. Leroi and Lyketsos (2005) assert that depression is represented in 24 percent to 32 percent of cases related to Alzheimer’s disease. Additionally, 17 to 27 percent of cases represent anxiety; over 41 percent of cases indicate apathy while delusions make up 23 percent of the cases. The symptoms are specifically recognized as dangerous when they begin interfering considerably with social and operational tasks, or when being identified by external parties who realize that the symptoms are progressing and that an indictment of dementia is acceptable. Additionally, changes in emotions are ordinary. This is identified by the prevalence in cases of depression and other emotional disorders. Gauthier, (2008) asserts that assessing dementia includes following a process that comprises distinguishing the syndromes of dementia for other maladies that are able to copy them such as delirium and mild cognitive disability and diagnosing a subtype in order to verify the type of treatment required. Diagnosing Alzheimer’s disease involves following a sequence of important phases that are intrinsic of determining the illness in an individual. The foremost phase in diagnosis of Alzheimer’s disease involves assessing the victim’s history. The history should comprise credible information received from the victim. After assessment of the victim’s history, an assessment based on the mental state of the individual is performed. The mental state appraisal comprises an authenticated cognitive function analysis. The final stage involves conducting a physical examination by focusing on neurological and vascular symptoms, which are complemented by investigations. Summary It is my belief that the literature review provided has shown the need for further research in the area of Alzheimer’s disease The gap in the literature is understandable in which my proposed research will address the etiology as well as the effects of Alzheimer’s disease. Extensive research has been carried out on Alzheimer’s disease based on its etiology, pathogeny, epidemiology, heredity, mannerism, medication, psychology and the effects it exemplifies on the victims who are considerably older people. Accordingly, the considerable effects of the disease has led to physicians and medical researchers alike to deduce innovative methods that assist in combating the ailment through the principles of prevention and cure. Overtime, Alzheimer’s disease has continued baffling the findings and conclusions of research and the strenuous efforts exuded by physicians and researchers. Regardless of the tenacity of the illness on aging people, innovations in medical technology have made it possible to mitigate the disease and the risks associated with it by providing methods and procedures that are effective and efficient in waging and prolonging the war against Alzheimer’s disease. The causative features of Alzheimer’s disease are currently unknown. However, research on the causes of the disease has identified several factors that are associated with acquisition of the disease. These factors are based on sociodemographics such as age and sex, genetic contribution factors such as family hereditary, medical records and treatment, which includes head injuries, vascular attacks, depression and Herpes Simplex, Habits, which include alcoholism and smoking, and insufficient physical and cognitive performance. In conclusion, research on Alzheimer’s disease has paved way for understanding and developing the pathology and treatment of the disease among aged people. Nevertheless, research in the ailment has also been conducted in the areas that involve prevention of the disease in order to prevent further financial and emotional distress on health care providers and family alike. Based on research evidence, preventive interventions have been deduced that actually restrict or delay the inception of Alzheimer’s disease. However, such interventions are either too complex to articulate or prevent the onset on a small-scale level thus lessening the impact. In general, Alzheimer’s disease is on the verge of elimination and thus it is important to continue further research in order to ensure that the disease is eliminated in totality from the society. Works Cited Brayne C. The Elephant in the Room-Healthy Brains in Later Life, Epidemiology and Public Health. Nature Reviews Neuroscience.8 (2007):233-9. Print. Burns, A., and J. O’Brien. â€Å"Clinical Practice with Anti-Dementia Drugs: a Consensus Statement from British Association for Psychopharmacology.† Journal of Psychopharmacology. 20.6 (2006): 732-755. Print. Burns, Alistair S. Severe Dementia. Chichester: John Wiley Sons, 2006. Print. Cooper, J.M, M.F. Shanks, and A.Venneri. â€Å"Provoked Confabulations in Alzheimer’s Disease.† Neuropsychologia. 44.10 (2006): 1697-1707. Print. Delavande, A, M.D Hurd, P Martorell, and K.M Langa. â€Å"Dementia and Out-of-Pocket Spending on Health Care Services.† Alzheimer’s Dementia: the Journal of the Alzheimer’s Association. 9.1 (2013): 19-29. Print. Ferri, Cleusa P, Martin Prince, Carol Brayne, Henry Brodaty, Laura Fratiglioni, Mary Ganguli, Kathleen Hall, Kazuo Hasegawa, Hugh Hendrie, and Yueqin Huang. â€Å"Global Prevalence of Dementia: a Delphi Consensus Study.† The Lancet. 366.9503 (2006): 2112-2117. Print. Gauthier, Serge. Clinical Diagnosis and Management of Alzheimer’s Disease. New York: Informa Healthcare, 2008. Print. Leroi, I. and C. Lyketsos. â€Å"Neuropsychiatric Aspects of Dementia†. Dementia. Eds. A. Burns, J. O’Brien, D. Ames. London: Hodder Arnold, 2005: 55-64. Print. Nestor, Peter J, Philip Scheltens, and John R. Hodges. â€Å"Advances in the Early Detection of Alzheimer’s Disease.† Nature Reviews Neuroscience. 10.7 (2004). Print. Reitz, C, B Patel, and J.A Luchsinger. â€Å"Relation between Vascular Risk Factors and Neuropsychological Test Performance among Elderly Persons with Alzheimer’s Disease.† Journal of the Neurological Sciences. 257 (2007): 194-201. Print. Spaan, Pauline, Jeroen Raaijmakers, and Cees Jonker. â€Å"Alzheimer’s Disease versus Normal Ageing: a Review of the Efficiency of Clinical and Experimental Memory Measures.† Journal of Clinical and Experimental Neuropsychology. 25.2 (2003): 216-233. Print. Strozyk, Dorothea, Dennis W. Dickson, Richard B. Lipton, Mindy Katz, Carol A. Derby, Sunhee Lee, Cuiling Wang, and Joe Verghese. â€Å"Contribution of Vascular Pathology to the Clinical Expression of Dementia.† Neurobiology of Aging. 31.10 (2010): 1710-1720. Print.