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Alzheimer's - Current research and treatments Alzheimer’s disease is a progressive form of Dementia. The diseases usually become fatal brain diseases that are manifested in influencing major brain function such as thinking memory and overall personality…
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Alzheimers - Current research and treatments
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Download file to see previous pages Beta amyloid protein damage cells by converting oxygen into hydrogen peroxide ‘bleach’ that corrode brain cells, interfere with message relays in the brain and signaling the cell to self-destruction (Patterson et al 120). In accordance to Patterson, Feightner and Garcia, there is a transition from epidemiologic observation to rigorous clinic test trials on Alzheimer’s patients which is crucial in understanding the most beneficial treatments amyloid Hypothesis is undergoing analysts alongside many trails aimed at reducing amyloid and plague which are completes and are in testing phases. Ways researched and documented are; anti aggregation agents, immunotherapeutic trials and modulation of secretases used in beta amyloid production. The major therapies of hyper-phosphorylated tau and novel targets are under research these therapies target the enhancement of serotonin receptor, factors of nerve growth, mitochondrial function enhancement, and advanced gyration products receptor. Boothby and Doering articulate that Current scientific research and the treatment of Alzheimer’s ‘covers four core areas. First is to increase efficiencies of damaged nerves, donepezil hydrochloride and memantine hydrochloride drugs are used. They foster the cell efficiencies though their effect is short lived. Secondly, is inhibiting manufacture of beta amyloid proteins. Current experiments are performed to determine a molecule that prevents the process of the parent beta amyloid protein (Patterson et al, 120). This is aimed at reducing the production of these proteins. Subsequently a lots of research work concentrates on ways of inhibiting beta amyloid build up within cells. Patterson, Feightner, and Garcia Scientists theorize that the beta amyloid become toxic with each build-up, thus if broken down at an earlier stage, they become less toxic. Lastly, clinical studies are aiming at shielding nerve cells form hydrogen peroxide effects. Use of vitamin E as a shield shows little but impacting improvement in a group of Alzheimer’s patients. A range of antioxidants is being tested in research labs to determine if they can protect the cells. Though minerals such as copper iron and zinc metals are essential for brain functions, there is continued research on ways to prevent the minerals interacting with brain cells. Though treatments may be available, it is paramount to see that the disease risk factors are discovered and prevented. Such risk factors are cholesterol, high blood pressure, Diabetes, gender hormones, brain activity, physical activity and antioxidants and nutrition. Research shows that cholesterol increases the blood pressure hence aggravating the risk of blood pressure. Statin drugs are used to lower blood cholesterol though clinical studies depict them as ineffective if used over a long period. Alternative research studies have shown that amino acid homocsyteine increase the risk of developing Alzheimer’s. Meanwhile, High blood pressure has a link between stroke and Alzheimer’s disease. High blood pressure damages blood vessels hence reducing the brain oxygen supply (Neugroschl and Sano 129). The Resultant 'oxidative stress' speeds up the production of amyloid protein. Subsequently, Diabetes is majorly associated with different type of dementia i.e. Alzheimer’s and vascular dementia. Both Diabetes and Alzheimer’s manifest similar characteristics in the elderly, that is deposits of amyloid protein in brain and pancreas. Women possess ...Download file to see next pagesRead More
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