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Alzheimer’s Disease Management Among Senior Citizens, Research Paper Example

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Research Paper

The human health has a natural tendency for deterioration with age, and senior citizens in any state are posed at greater risks for health stemming from the biological decline of their organisms’ vitality. Among the most common diseases posing the serious public health burden on the global population, one should note the Alzheimer’s disease – the most common neurodegenerative disease known up to date also defined as the most common cause of dementia among elder people (Milone 991). Since AD is usually associated with the increasing age, the aging of the global population is at present closely related to the number of AD patients, causing major public concerns; moreover, the increasing number of AD co-morbidity and risk factors is alarming.

Alzheimer’s disease (AD) is a neurodegenerative disorder that occurs insidiously, and develops progressively with age (Massano 34). The emergence of AD is usually associated with the neural degeneration resulting from deposition of amyloid β1-42 peptide and hyperphosphorylated tau protein in the human brain; the areas affected by neuronal damage caused by AD usually include hippocampus and other medial temporal lobe structures responsible for memory and cognition (Massano 34). Ritsner also cited the recent research findings relating the vascular pathology and typical Alzheimer’s disease pathology, which suggests that the mentioned disorders are biologically related (Ritsner 521).

The increasing number of AD patients poses an additional strain on the governmental resources in the USA; as Turkington and Mitchell admitted, although AD patients account for only 13% of Medicare population, total spending on their needs equaled 34% of Medicare spending in 2005 (137). The authors also cite the data from the Centers for Disease Control and Prevention to admit that Medicare spending on AD patients equaled $91 billion in 2005 (Turkington and Mitchell 137). At present, Medicare services cover such reasonable expenses as evaluation and management visits by doctors; physical, occupational, and speech therapy; psychotherapy and behavior management therapy; and home health care in case the patient is homebound. However, Medicare does not cover such services as drug prescription, adult day care, room and board in assisted living institutions, custodial care expenses in nursing homes, and personal home care (Turkington and Mitchell 137).

Hence, as one can see, there is an increasing financial and public health threat stemming from the rising number of patients diagnosed with AD. Understanding that this disease is directly correlated with patients’ age opens new avenues for comprehending the nature of AD, and identifying the risks of senior citizens’ having co-morbidities. Research evidence suggested that there is a direct relationship between acquiring AD and having diabetes mellitus type 2, the level of cholesterol, and the presence of a cognitive and memory decline. Hence, the present interrelationships have to be analyzed in order to present a clearer image of AD occurrence, its mitigating and risk factors.

The relationship between the level of cholesterol and Alzheimer’s disease was researched by Shobab, Hsiung, and Feldman; Simons, Keller, Dichgans, and Schulz; and Vaya and Schipper. Shobab et al. stated that among the pathogenic factors affecting the AD risk and expansion, cholesterol is one of the most prominent contributors (841). The excessive presence of brain cholesterol was clinically found correlated with the formation and deposition of amyloid-β peptide from the amyloid precursor protein – the brain chemical commonly known as almost solely responsible for the development of AD in a human brain (Shobab et al. 841). Vaya and Schipper supported that relationship by indicating that aberrant cholesterol metabolism is commonly observed in AD and other neurological diseases (1727). The researchers saw a clue to understanding the connection of cholesterol and AD in the Oxysterols and other cholesterol oxidation products that act as ligands of liver X activated receptor (LXR) nuclear receptors responsible for the regulation of genes controlling the homeostasis of cholesterol in the human organism. Hence, researchers clinically proved that the activation of oxysterol-mediated LXR causes the overall cholesterol redistribution and removal from the human organism, and the function of LXRs is in conducting neuroprotection (Vaya and Schipper 1727).

Simons et al. also saw the link between cholesterol levels and AD development; the authors claimed in their study that amyloid-β peptide is derived from the proteolytic cleavage from the amyloid precursor protein (APP), while epidemiologic and biochemical evidence suggests a link between APP processing, cholesterol, amyloid-β peptide, and AD (1089). The authors cited recent research evidence that cholesterol-reducing drug intake among elder people is commonly associated with the reduced risk of AD acquisition, mainly because of these drugs’ capability to inhibit the 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMG-CoA reductase inhibitors or statins) (Simons et al. 1089). Vaya and Schipper proposed the use of synthetic oxysterol-mimetic drugs to activate LXR receptors within the CNS as a type of AD management, in case AD is perceived as a disease characterized by “deranged tissue cholesterol homeostasis” (1727).

An explicit link between AD development and the diabetes mellitus diagnosis has also been established. Milone indicated that epidemiological data suggested the risk of diabetes to increase the probability of AD development. According to the researcher’s observations, diabetic subjects increasingly showed the symptoms of cognitive dysfunction, leukoariosis, and severe hippocampal atrophy (Milone 991). Among other clinical observations, Milone noted,

“Neuritic plaques and neurofibrillary tangles, the pathological hallmarks of AD, accumulate more abundantly in the brains of diabetic patients relative to control subjects. The association between diabetes and AD pathology seems even stronger among carriers of the apolipoprotein E ε4 allele, a variant that by itself carries an increased risk for AD” (Milone 991).

The connection between diabetes and AD was also seen by Shah, DeSilva, and Abbruscato who noted the occurrence of altered brain glucose in both diabetic and AD patients (12629). The authors clarified that glucose traditionally enters the human brain through the glucose transporters present in the blood-brain barrier. Hence, even the slightest changes in the glucose transporters are likely to cause a serious dysfunction in the brain glucose homeostasis. Though the researchers did not manage to understand the nature of the glucose transporters’ change causing both diabetes and AD, they have postulated that “future recognition of the role of new glucose transporter isoforms in the brain may provide a better understanding of brain glucose metabolism in normal and disease states” (Shah et al. 12629). Therefore, more research attention should be paid to glucose transportation mechanisms and metabolism, which may shed light on the etiology of both diseases.

Finally, the relationship of the cognitive decline and AD development is of obvious interest, since many researchers associate AD diagnosis with old age, and declining cognitive and memory capacities. Hughes published research findings on the ways of sustaining high-quality cognitive activity even at an old age, which is likely to help individuals avoid AD development. The author called AD the most common type of dementia – “a chronic syndrome characterized by acquired cognitive deficits in more than one cognitive domain, currently including memory, that are severe enough to affect daily (social and occupational) functioning” (Huhes 112). Hughes found out in her literature review that prospective studies of cognitive activity and risk of cognitive impairment and dementia established a close link between reduced rate of cognitive decline and reduced risk of dementia, AD, and cognitive impairment (Hughes 113). The present evidence suggests that cognitive decline goes hand in hand with AD, and patients with mild cognitive impairments and AD may highly benefit from cognitive training strategies (Hughes 115).

There is growing evidence suggesting the connection between nutritional habits, cognitive decline, and AD development. It is obvious that people who have unhealthy nutritional preferences over a long period of time do not receive adequate amounts of nutrients traditionally seen as responsible for cognitive capacity, such as inadequate intake of folic acid, vitamin B6, B12, which causes the elevated levels of homocysteine (Ritsner 521). The regular deficiency of the indicated nutrients in the human organism is harmful for the memory, cognition, and overall brain function because of the direct participation of the named substances in the memory and cognitive performance. Thus, provision of sufficient nutrients to support the memory function is vital for the prevention of AD, since, as Massano admitted, AD starts with memory difficulties, many years before the cognitive and functional declines are manifested (34).

The evidence presented above implies that AD poses a serious financial, physical, and psychological burden on the individuals diagnosed with AD, their families, and the state in which they live. The costs for AD management in the USA are growing from year to year, and the government seeks new ways of rearranging the provision of AD care so that to achieve a cost-efficient strategy of care. However, the present effort does not change the real-life epidemiology of AD – the overwhelming portion of AD patients are people older than 65, which creates the need for more specialized geriatric care for them. AD patients, as the present paper showed, have an increased risk for cognitive and memory decline, mounting cholesterol levels, and diabetes, which requires more specific care for them in medical terms. However, one can make other conclusions from the analysis of clinical evidence in the present work – that nutritional habits of people at a younger age may affect the risk of AD development, and people with diabetes should take closer care of their health and undertake more active cognitive activity, which is likely to protect them from the onset of AD.

Works Cited

Shah, Kaushik, Shanal DeSilva, and Thomas Abbruscato. “The Role of Glucose Transporters in Brain Disease: Diabetes and Alzheimer’s Disease”. International Journal of Molecular Sciences 13 (2012): 12629-12655. Print.

Milone, Margherita. “Mitochondria, Diabetes, and Alzheimer’s Disease”. Diabetes 61. 5 (2012): 991-992. Print.

Vaya, Jacob, and Hyman M. Schipper. “Oxysterol, Cholesterol Homeostasis, and Alzheimer Disease”. Journal of Neurochemistry 102 (2007): 1727-1737. Print.

Simons, Mikael, Patrick Keller, Johannes Dichgans, and Jorg B. Schulz. “Cholesterol and Alzheimer’s Disease: Is There a Link?”. Neurology 57 (2001): 1089-1093. Print.

Shobab, Leila A., Ging-Yuek R. Hsiung, and Howard H. Feldman. “Cholesterol in Alzheimer’s Disease”. Lancet Neural 4 (2005): 841-852. Print.

Hughes, F. Tiffany. “Promotion of Cognitive Health Through Cognitive Activity in the Aging Population”. Aging Health 6. 1 (2010): 111-121. Print.

Ritsner, S. Michael. Brain Protection in Schizophrenia, Mood, and Cognitive Disorders. New York, NY: Springer, 2010. Print.

Massano, Joao. Cognitive Impairment and Dementia – an Update. Switzerland: Frontiers E-Books, 2012. Print.

Turkington, Carol, and Deborah R. Mitchell. The Encyclopedia of Alzheimer’s Disease. 2nd ed. New York, NY: Infobase Publishing, 2010. Print.

Outline

  1. Introduction – overview of aging and health
  2. Alzheimer’s disease – definition, causes, severity
  3. Burden of AD on the public health and spending
  4. Connection of AD and cholesterol level
  5. Connection of AD and diabetes
  6. Cognitive activity, dementia, and AD
  7. Care for AD patients and the need to reconsider the public health burden of AD
  8. Conclusion

 

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