Alzheimer's Disease Issues - Case Study Example

AR Alzheimer Disease 5/25 Alzheimer Disease Brain is known to be the control centre of the bodily functions and activities of a human being. It is designed in such a way that impulses pass in the brain through neurons which then electrically stimulate parts of brains. These parts of brains then send out impulses again to the specific organs where a reflex action is required. Cerebral Cortex is a part of the brain which primarily is related to intelligence and cognitive abilities of an individual. Several diseases may arise if this part of the brain is affected and one such disease is Alzheimer Disease. Alzheimer is mostly seen in individuals who are above the age of forty five and it principally develops into dementia in its latter stages. It is characterized by loss of cognitive abilities which occurs due to the loss of normal brain functions. In the latter stages of Alzheimer Disease the sufferer becomes totally disoriented and shows memory loss such that he is not able to recognize his very close family members. (Evans et al, 1989; Gao et al, 1999). The primary feature of Alzheimer Disease is the atrophy of the cortex. But in some cases it is seen that neuritic processes may accumulate, abnormalities in cerebral nucleus may occur or amyloid angiopathy may be seen. It is seen that Alzhemier Disease does not show any symptoms early at age but after a person reaches 50 the symptoms become obvious. As an individual ages the chances of the disease increase even more often reaching to a level of 40% in individuals who are in their eighties ((Evans et al, 1989; Gao et al, 1999; Strauss et al 1999 ). Studies on the disease have shown that cortical atrophy is the major cause of the disease. The cerebral sulci become more prominent in the temporal, frontal and parietal lobes. To cover up for this atrophy usually the ventricle in the brain enlarges. Microscopic studies have shown that neuritic plaques and neurofibrillary tangles accumulate along with amyloid angiopathy. Neuritic plaques are spherical neuritic processes which surround the central amyloid core in Alzheimer. Neurofibrillary tangles are a group of filaments which are found in the cytoplasm of the neurons that usually surround the nucleus. Amyloid angiopathy is a sign of Alzhemier Disease but it can also be found in other diseases. It is believed that Alzheimer later progresses to dementia in individuals because of loss of choline accetyltransferase, synaptophysin immunoreactivity and loss of synaptic transmission. It is believed that Alzheimer is primarily caused by a protein known as Aβ. Aβ is difficult to be degraded and is hence known to possess the properties to be neurotoxic. This protein is believed to be synthesized by the processes done by APP. APP is also a protein which is found on the cell surfaces. Normally APP is cleaved by an activity known as α-secretase activity. This α-secretase activity cleaves APP after which APP cannot form the neurotoxic Aβ protein. In Alzheimer much of this APP is endocytosed after which it undergoes several processes to form the neurotoxic protein (Mumm 2000). The enzymes which carry out these processes are BACE-1 or β secretase and γ-secretase. β secretase acts on the APP in transmembrane domain whereas γ-secretase acts on the APP which is inside the transmembrane domain. Alzheimer is also believed to have genetic influences because of which APP secretes this neurotoxic protein. Three of the recognized genes which code for APP are found on chromosome 21, 14 and 1. (42) Mutations can also cause Alzheimer Disease and it is known that a mutation in a gene on chromosome 19 can increase the risk of Alzheimer (Strittmatter et al 1993). The question now stands as to why Alzheimer disease onsets in an individual. To answer this question many aspects of the disease are analyzed. Nutrition is presumed to be directly related to the onset of Alzheimer’s disease. Research done on the relation of the nutritional status of an individual has shown that Vitamin D may have a direct relation with the onset of Alzheimer. A research by Dr Grant proves that Alzheimer’s may be related to low serum levels of Vitamin D. It is said by Dr Grant that old people usually have the deficiency of Vitamin D because of which dental caries, diabetes mellitus and depression may arise in individuals. And all these diseases together are presumed to be a cause for Alzheimer Disease. Relating nutrition to Alzheimer has paved way for many researches to be done on this issue (Drug Week, 2009). Such a research was done to find the relation between folate and the risk of Alzheimer Disease. It was seen in this research that individuals who consumed folate were greatly reducing the risk of acquiring Alzheimer Disease. The incidence rate was calculated to be 45% as the individuals consuming folate were decreasing their risk of acquiring Alzheimer by 55%. The research compared the individuals who were taking folate regularly to those who were not and it was found that it had a relation with the onset of the disease. It was also found that Vitamin C or B12 had no such direct relation with decreasing the risks of acquiring the disease (Folate may lower Alzheimers risk, 2005; Vitamins unlikely to revitalize the mind, 2010). Another such research found a link between the consumption of vegetable and fruit juices with Alzheimer Disease. It was successfully found that an antioxidant called polyphenol is playing a role in reducing the risk of acquiring the disease. And this antioxidant is found in fruit and vegetable juices thus it was concluded that people who regularly had vegetable and fruit juices had less probability of catching the disease (Fruit juice may cut Alzheimers risk, 2009). Amino Acids are known to be the basic functional units of proteins and their presence in human body is of crucial importance to their health status. However an amino acid called Homocysteine is known to play significant role in the onset of Alzheimer Disease. According to the researchers it is believed that homocysteine circulates in the body much more than what is needed. To reduce the level of homocysteine circulating in the body it is proposed by the researchers that vitamin supplements be given to the individuals. These vitamin supplements would help to methylate homocysteine into cysteine and would thus help to reduce the circulating levels of homocysteine in the body. Reducing the levels of circulating homocysteine would help in reducing the risks of Alzheimer Disease. However this hypothesis is yet to be proved by other researches as vitamin supplements are believed to have no net effect on cognitive impairment. Research on this topic has almost always proved to be a failure as the Alzheimer patients show no improvement in their cognitive skills (DAnci, 2008). Another research relating nutrition to Alzheimer Disease was done on the consumption of Mediterranean diet. It was seen that patients who were suffering from disease and were consuming Mediterranean diet properly had a greater chance of survival than the ones who were not. It was also evaluated from the research that individuals who were consuming the diet decreased their progression of disease to its latter stages. The mortality rate in these individuals was decreased than the ones who were not consuming the diet. It was hence concluded from this research that Mediterranean diet could be of great use to patients who were suffering from Alzheimer Disease (Davis, 2007). Not only is nutritional status related to decrease the levels of risks to acquire Alzheimer but it is also related to increase the levels of risk. Saturated fats and copper are known to be one of the factors which increase the levels of risk of acquiring Alzheimer in an individual. But it was researched that only those individuals showed loss of cognitive abilities who consumed high levels of copper and saturated fats together. Individuals who consumed high levels of copper but did not consume high levels of fat did not show loss of cognitive abilities. Thus it is recommended that individuals avoid a diet which has a high level of copper and fat both (Too much copper and fat could lead to AD, 2006). It has been found that hormones and Alzheimer Disease may also have something in common. An effect on insulin has been recently studied which is somehow linked to the onset of the grave disease. Insulin is a hormone secreted by pancreas which helps in the absorption of glucose in the cells. Diabetes and Alzheimer Disease have been linked together. A new and interesting finding by the researchers at the US Brown Medical School indicated the prevalence of a third type of diabetes which was classified as type 3 diabetes. It has been discovered that apart from the pancreas the brain also works towards the secretion of insulin. This insulin works as a regulator of the metabolism of glucose mainly in the brain and does not mainly have an effect on the body blood glucose levels. The neurologic cells of the brain are not able to maintain normal function in the absence of this insulin which leads to loss of function of the brain cells. This accounts for Alzheimer’s disease and a link has been found out between diabetes type 3 and this neurological condition (BBC News, 2005) Estrogen another hormone in women is known to have a direct link with Alzheimer Disease in women. It is known that hormone therapies in women have helped them to cope up with the early onset of Alzheimer Disease. But a research done showed that if women had hormone therapy for a long time then they might develop greater risks of acquiring Alzheimer Disease (Exercise, estrogen, and executive function, 2008). Different treatment strategies have been sought for the management of Alzheimer Disease. It has been known to no perfect cure of the disease is still provided by the medical professionals however it can be managed by certain drugs and types of interventions. The drugs which are generally prescribed to people with Alzheimer Disease are Cholinesterase Inhibitors and partial glutmate antagonists. The cholinesterase inhibitors act on the cholinesterase enzyme which helps in the breakdown of acetylcholine. This helps to build up excess acetylcholine (a hormone) which is believed to play significant role in the building up of memories. Rivastigmine, galantamine donepezil hydrochloride are three types of cholinesterase inhibitors which are being widely used by physicians to manage Alzheimer. Glutamate is also believed to exert stress on the brain and thus it is recommended that glutamate be reduced in the individuals who suffer from Alzheimer. Partial Glutamate Antagonists help to inactivate the neurotransmitter Glutamate so that it cannot activate many nerve cells. Memantine is one example of a partial glutamate antagonist. Still other treatment strategies are also used which do not involve the usage of medicines such as therapies. Patients with Alzheimer are encouraged to take part in these therapies through which they can interact and build upon their cognitive skills. Patients with Alzheimer are encouraged to dance, sing and talk so that the brain does not lose its capability to think. Similarly they are also recommended specific dietary schedules which they should follow in order to slow down the progression of Alzheimer as mentioned above (Katzung et al 2008; Rang 2007). In conclusion it can be said that Alzheimer Disease is a disease which causes loss of cognitive abilities because of cortical atrophy. Its onset is linked to both nutrition and hormonal imbalance. Although the disease does not have any possible cure but it can be managed by certain therapies and medications. Further research is still needed to clarify the effects of both nutrition and hormones on the onset of Alzheimer Disease. Folate and other vegetable juices have proved to be very beneficial to reduce the risk of Alzheimer disease whereas copper and saturated fats are increasing its risk. The hormone insulin and estrogen are linked with Alzheimer Disease and to balance these hormones in the body it is necessary that extensive researches are carried out. (Exercise, estrogen, and executive function, 2008). Bibliography BBC NEWS . Study suggests type 3 diabetes. 2005. http://news.bbc.co.uk/2/hi/health/4315609.stm DAnci, K. (2008). Nutrition Updates. Nutrition Reviews, 66(12), 730-733. doi:10.1111/j.1753-4887.2008.00129.x. Davis, S. (2007). Mediterranean diet may slow advancement of AD. Geriatrics, 62(11), 13. Retrieved from Health Source - Consumer Edition database. Evans DA, Funkenstein HH, Albert MS, Scherr PA, Cook NR, Chown MJ, et al. (1989). Prevalence of Alzheimers disease in a community population of older persons. Higher than previously reported. JAMA : the Journal of the American Medical Association. 262 (18), 2551-6. Gao S, Hendrie HC, Hall KS, & Hui S. (1998). The relationships between age, sex, and the incidence of dementia and Alzheimer disease: a meta-analysis.Archives of General Psychiatry. 55 (9), 809-15. Top of Form Mumm JS, & Kopan R. (2000). Notch signaling: from the outside in. Developmental Biology. 228 (2), 151-65. Bottom of Form (2008). Exercise, estrogen, and executive function. Harvard Mental Health Letter, 24(8), 6. Retrieved from Health Source - Consumer Edition database. (2005). Folate may lower Alzheimers risk. Geriatrics, 60(10), 11. Retrieved from Health Source - Consumer Edition database. (2009). Fruit juice may cut Alzheimers risk. Mayo Clinic Health Letter, 27(2), 4. Retrieved from Health Source - Consumer Edition database Is Vitamin D Deficiency Linked to Alzheimer Disease and Vascular Dementia?: Hypothesis Explored in the Current Issue of the Journal of Alzheimer Disease. Drug Week. June 26 2009. Journal of Alzheimer Disease. Top of Form Strittmatter WJ, Saunders AM, Schmechel D, Pericak-Vance M, Enghild J, Salvesen GS, et al. (1993). Apolipoprotein E: high-avidity binding to beta-amyloid and increased frequency of type 4 allele in late-onset familial Alzheimer disease. Proceedings of the National Academy of Sciences of the United States of America.90 (5), 1977-81. Bottom of Form (2006). Too much copper and fat could lead to AD. Geriatrics, 61(11), 8. Retrieved from Health Source - Consumer Edition database. Top of Form von Strauss E, Viitanen M, De Ronchi D, Winblad B, & Fratiglioni L. (1999). Aging and the occurrence of dementia: findings from a population-based cohort with a large sample of nonagenarians. Archives of Neurology. 56 (5), 587-92. Bottom of Form Top of Form Bottom of Form (2010). Vitamins unlikely to revitalize the mind. Harvard Mental Health Letter, 26(8), 4-5. Retrieved from Health Source - Consumer Edition database. Top of Form Trevor, A. J., Katzung, B. G., Masters, S. B., & Katzung, B. G. (2008). Katzung & Trevors review of pharmacology. New York: McGraw-Hill Medical. Top of Form Rang, H. P. (2007). Rang and Dales pharmacology. Philadelphia, PA: Churchill Livingstone/Elsevier. Bottom of Form Bottom of Form Bottom of Form Top of Form Bottom of Form Read More