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2018년 3월 22일
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▣ My Essay     Ryan's Warehouse 2018.03.22. 21:28 (2018.03.22. 12:32)

THINKING ABOUT THE FUTURE OF ALZHEIMER’S DISEASE

Alzheimer’s disease By Ryan Berry
May 30th, 2014
Abstract
This following paper discusses the current state of Alzheimer’s disease. This paper talks about what little is currently known about this form of dementia. This paper also acknowledges current research and studies, what they are finding, and the potential impact they have on Alzheimer’s research and treatment.
 
It is only human to forget things like biology notes and homework, but what happens when the brains neurons face a merciless attack from an unstoppable disease; this is exactly what happens when Alzheimer’s strikes. Alzheimer’s disease, the most common form of dementia, stops brain function gradually reducing the victim to dependant and incoherent state. Alzheimer’s disease currently affects 35 million people worldwide (Thomson, 2014). Although there are many theories about the disease, and drugs are in circulation to try and counteract the detrimental symptoms; very little is known for sure about the disease. In 2010 Even diagnosis could only be accurate without doubt after a patient’s death and autopsy (New scientist, 2010).
 
Alzheimer’s disease is thought of scientifically as buildup of beta-amyloid and tau proteins which through various methods kill neurons in the brain (Thomson, 2014). Although they were not identified, these beta-amyloid and Tau proteins where first observed early in the 19th century by Alois Alzheimer, she noted plaques and silver tangles present in the brains of dementia patients (Hutchinson Dictionary of Scientific Biography, 2005) These proteins and are now the topic of many theories about the cause and progression of Alzheimer’s disease.
 
Beta-amyloid proteins are naturally present in the brain, but overproduction can cause toxic plaques to build up that coat parts of the brain and poison neurons eventually killing them. Some believe this is the cause of Alzheimer’s. However other research suggests that these plaques are not to blame. Some researchers look more favorably on the theory that tau proteins, which build up inside the brains neurons in the form of fibrous tangles which eventually kill the host neurons, are a more reasonable culprit. Research suggests that the quantity of tau protein tangles better correlates with the severity of dementia in an individual then the number and size of beta-amyloid plaques (New scientist, 2010).
 
One study in the United States has used fluorescent tracers detectible during brain scans to monitor the progression of tau tangles and beta-amyloid plaques as Alzheimer’s disease develops. Their research also suggests that the plaques associated with Alzheimer’s disease are largely harmless, but do serve as a catalyst to speed up the spread of Tau protein tangles. The study showed that Tau protein tangles showed up much later then the beta-amyloid plaques, but grew more quickly. They identified that the spread of Neuron killing tangles originated in the hippocampus and quickly spread outward. The hippocampus is often thought of as the memory center of the brain therefore this study would explain why early Alzheimer’s patients suffer memory loss while retaining body function until later (Coghlan, 2013).
 
Alzheimer’s disease usually strikes in the minds of the elderly. The chances of developing Alzheimer’s disease double every five years once the age of 65 is reached; at the age of 85 the probability of developing Alzheimer’s disease is nearly 50 percent (Tufts University Health & Nutrition, 2010). However one strand of Alzheimer’s has been known to strike at a healthy and young age; early on-set Alzheimer’s is rare and often associated with familial cases. One study has shown that a mutation on the S182 gene on chromosome 14 may be the culprit for up to 70 percent of all cases of early on-set Alzheimer’s (Seachrist, 1995).
 
Alzheimer’s disease is not thought to be contagious but studies have shown large concentrations of occurrences in certain families. One village in Research in this area has suggested that inherited mutations on the gene for apolipo-protein E on chromosome 19, as well as the gene for beta-amyloid precursor protein on chromosome 21 may play a role in familial cases (Seachrist, 1995).
 
Although scientists have yet to produce an Alzheimer’s immunization one study has observed evidence that points to a naturally occurring Alzheimer’s preventative. A gene referred to by the study as APP is responsible for synthesising the protein beta-amyloid, which is responsible for the plaques associated with Alzheimer’s. Researchers have discovered that when mutant APP from one parent mixes with normal APP from the second parent, it will reduce the risk of developing Alzheimer’s. However the same study observed that if a patient receives mutant APP genes from both parents it will promote and may even cause some cases of Alzheimer’s (New Scientist, 2009).
 
Due to how little is known about Alzheimer’s disease, present treatment is theoretical at best (Laber-Warren, 2012). Many treatments involve drugs to stop the growth of beta-amyloid plaques, unfortunately the plaques are usually present before the tau proteins tangles take affect and the patient starts to show symptoms. Once the patient shows symptoms and treatment is administered the beta-amyloid plaques, which serve only as catalysts for the tau protein tangles, are already present. This kind of treatment, in the ideal situation, does no more than slow the process (Coghlan, 2013).
 
The best results from existing measures come from patients who continue to Challenge themselves mentally. Patients who occupy themselves solving problems and puzzles, although still eventually succumbing to the same symptoms, are shown to deteriorate slower (Harvard Medical School, 2013).
 
Other scientists have started research into Alzheimer’s prevention opposed to treatment. Although none of their methods are proven. Their studies recommend regular physical activity not only at a young age, but continued in old age. This has to do with maintaining a healthy body, weight, and sweating out toxins. They also recommend a diet with lots of antioxidants, vitamin E and vitamin D, the latter of which may even help prevent build ups of beta-amyloid. Their study described the brain as “a site of high metabolic activity” making it vulnerable to oxidative damage and change in blood pressure. The study showed that a lifestyle designed to reduce heart problems would also reduce the risk of Alzheimer’s and other forms of dementia (Tufts University, 2010).
 
While these studies look into ways to discourage Alzheimer’s from developing another study at Harvard University is looking into ways to halt and maybe even reverse Alzheimer’s disease. While others drugs focus on antibodies, combatting the growth of plaques, this study has focused on the source. Research has showed that copper and zinc, naturally found in the brain, are fueling both the amyloid plaques and tau protein tangles growth. Several scientists at Harvard have developed a drug called PBT2 (currently in beta phase testing) which prevents the metals in the brain from being used by the plaques and tangles alike and leaving it to be used for essential functioning in the brain. The drug also promotes the growth of new neurons in the hippocampus to replace the dead ones, and improve function. Although still in testing this drug is showing much promise on improving test subjects’ brain and body function (Harvard Medical School, 2013).
 
Alzheimer’s is a critical disease that not only kills, but is on the rise as our population ages. Although the secrets of how Alzheimer’s disease takes root and destroys a human brain are still elusive, scientists around the world continue to dedicate themselves to it. Although very little research has been proven at this point it is all we can do to keep studying, keep seeing new patterns, and keep trying new things. As our doctors are able to treat different diseases in new ways every year, hopefully one day our minds will be safe from Alzheimer’s disease.
 

 
References
Coghlan, Andy (2013). Alzheimer's growing in a living brain. New Scientist, 219 (2936) 16-16.
Harvard Medical School (2013). Can we reverse Alzheimer's? New approaches from Harvard offer hope. Harvard Health Letter, 38 (3), 1-2.
Hutchinson Dictionary of Scientific Biography (2005). Alzheimer, Alois (1864 - 1915). Hutchinson Dictionary of Scientific Biography p1.
Laber-Warren, Emily (2012). Early Treatment for Alzheimer's. (Cover story). Scientific American, 307 (6), 38-39.
New Scientist (2009).Too much of a good gene. New Scientist, 201 (2700) 13-13.
New Scientist (2010). Alzheimer’s unlocked. New Scientist, 207 (2770) 2-2.
Seachrist, L (1995). Gene for early, aggressive Alzheimer’s. Science News, 148 (2) 23-23.
Thomson, Helen (2014). A test to see if you will get Alzheimer’s. New Scientist, 221 (2960), 12-12.
Tufts University (2010). The Battle for your Brain. Tufts University Health & Nutrition Letter, 28 (8), 1-4.
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