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Why Is There No Cure for Alzheimer’s Disease?

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This project aims to find out why there is no cure for Alzheimer’s disease. I plan to investigate and analyse advantages and disadvantages of contributing factors to the disease and what could trigger the symptoms of the disease. Through these, I can decide whether there is a possible cure for the disease. I chose to complete a project about the disease because I find it to be an interesting topic, particularly as the disease has being deemed ‘irreversible’ and not seen as a normal part of the ageing process.

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I always thought that ‘forgetting’ was a normal part of ageing, meaning everyone will fall to this fate as they grow older. However, I did not know that forgetfulness can become a disease. On watching a popular medical show ‘Grey’s Anatomy’; Alzheimer’s disease came to my attention as being a personal struggle which has a devastating impact on family and friends therefore I chose to concentrate on reasons why there is no cure for the disease and possible ways to prevent acquiring the disease.

Alzheimer’s disease is most commonly known as a neurodegenerative disease, which put simply is a death to the nerve cells in the brain; there is a progressive loss of structure and function of the neurons characterized by impairment of memory and thought but which eventually causes disturbances in reasoning, planning, language, and perception. Alzheimer’s is deemed an ‘irreversible disease’ but this does not mean it cannot be treated. While the disease can occur in younger people, even in their 30’s and 40’s, the risk is higher in those aged after 65.

One in ten people aged over 65 have Alzheimer’s disease while 1 in five people aged over 85 have Alzheimer’s disease. The rate of occurrence of the disease increases exponentially with age, which means that it occurs very rarely among those 40-50 years old, increases between 60 and 65 years, and is very common over 80 years. It is estimated that there are currently about 18 million people worldwide with Alzheimer’s disease. This figure is projected to nearly double by 2025 to 34 million. Much of this increase will be in the developing countries, and will be due to the ageing population.

Currently, more than 50% of people with Alzheimer’s disease live in developing countries and by 2025, this will be over 70%. Other risk factors besides age are: family history of Alzheimer’s, stress, serious illness or injury, inadequate physical and social activity, poor diet, perhaps even race. Findings of a 1998 study of 1,000 people in New York, reported by the Alzheimer’s Association, suggest that the risk of Alzheimer’s is four times higher for African Americans, and twice as high for Hispanics as for white Euro-Americans.

A neuron is the building block of the nervous system; neurons transmit information from our environmetal stimuli throughout the body. In the brain, there are about “100 billion nerve cells” all connecting together to form communication networks; this enables our body to respond the way it does; according to what function each groups of nerve cells are involved in. These nerve cells communicate information to the brain in both chemical and electrical forms. The dendrites of the neuron receive information from the sensory receptors or other neurons which is passed down to the cell body of the neuron and then the axon.

Once its arrived at the axon, it travels down the length of the axon in the form of an electrical signal known as an action potential ( this occurs when a neuron sends information down an axon, away from the cell body). Once the information has reached the end of the axon, it must be transmitted across the synaptic gap to the dendrites of the other neuron. In some cases, the electrical signal can almost instantly bridge the gap between the neurons and continue along the path.

And, in other cases, neurotransmitters which are chemical messengers will be needed to send the information from one neuron to the next, this would be done by releasing the chemical messengers from the axon terminals to cross the synaptic gap so to reacch the receptor sites of the other neuron. In a process known as reuptake, these neurotransmitters attach to the receptor site and are reabsorbed by the neuron to be reused. The neurotransmitter, Acetylcholine is associated with memory, muscle contractions, and learning. A lack of acetylcholine in the brain is associated with Alzheimer’s disease.

In order for communication to happen, the neurons need to transmit information from one neuron to another neuron; a break in this communication chain would result in information not been passed to the brain in order for a response. Neurons are different from some other body cells because they stop reproducing shortly after birth. This means that we would have more neurons at birth than later in life, as some would die during our life cycle but they will not be replaced. Alzheimer’s disease is not a normal part of ageing, this is because, it is a disease that refers to a decline in the ognitive function of the brain, affecting with daily life and activities. This disease starts in the region of the brain that affects recent memory and then it spreads to other parts of the brain. There is treatment that can slow the progression of the disease and help manage its symptoms in some people, so it is not inevitable stage in a person’s life. This would help me investigate the main causes of the disease and I will be investigating the contributing factors that will increase an individuals chanceof acquiring Alzhiemer’s disease.

Also, I will be investigating ways in which an individul can reduce their chance of acquiring Alzheimer’s disease. ABSTRACT Alzheimer’s disease is most commonly known as a neurodegenerative disease, which is as a consequence of nerve cells in the brain dying. This erosion causes a progressive loss of structure and function of the neurons characterized by impairment of memory and thought, but which eventually causes disturbances in reasoning, planning, language, and perception. Alzheimer’s disease is deemed to be an irreversible disease and so this project aims to investigate whether there can be a possible cure for the disease.

Using secondary research, I have investigated and evaluated contributing factors and possible preventions which could answer the question, “Why is there no cure for Alzheimer’s disease”. Using secondary research, I have gained an insight into beliefs and concerns of patients and their families, but also of researchers trying to find links for a possible cure of the disease. The main arguments against there not being a cure for the disease include there not being a direct known cause of the disease, what the symptoms of the disease are and how to reverse those symptoms.

However, opponents argue that the reason why there is no cure is due to the governments not putting enough finance into researching the links and causes in order to educate the population. My opinion is that a solution can be found to cure Alzheimer’s disease but is reliant on increases financing. LITERARY REVIEW The Question that this project aims to answer is: Is there is any hope for a possible cure of Alzheimer’s disease in the future? This section of the project focuses on research into what the world has proposed as possible risks, prevention or cures for Alzheimer’s disease.

The discussion section of the project will give a clearer view into the findings from the research. Alzheimer’s disease has an increasing effect on the world population, yet there are only two known possible causes: Age and Genetic Predisposition. Genetic predisposition refers to genes an individual has which makes them more likely to develop the disease. Often, these genes need a trigger. According to the World Health Organisation, it is a fact that the rate of occurrence of Alzheimers disease increases exponentially with age, which means that the symptoms worsen with age.

Therefore, an increasing number of people are worried about their chances of getting the disease which is now what Dharma Singh Khalsa argues is ‘the sixth leading cause of death in the world, surpassing diabetes’. It seems that not only people over 65 years of age should be worried about developing the disease, but also those in their 20’s and 30’s should also be concerned as more people are increasingly diagnosed with Alzheimer’s disease at such early ages. Indeed Dr. Dharma Singh Khalsa reports that, “Last year, over 500,000 people younger than 65 were diagnosed with Alzheimers — some of them in their 20’s and 30’s”.

In this research he argues that the likelihood of developing Alzheimers doubles every five years after age 65. This strengthens the idea that age is a contributing factor to acquiring the disease. However, Howard Fillit, M. D. argues that “Less than 1% of people under the age of 65 get Alzheimer’s disease” suggesting that people under the age of 65 are less at risk. An individual’s geographical location has been argued as being a contributing factor to acquiring Alzheimer’s disease. Urban areas such as cities, towns or conurbations, are characterized by higher population density and vast human features in comparison to areas surrounding it.

Rural areas (the country) are not urbanized, though when large areas are described, country towns and smaller cities will be included. They have a low population density, and typically much of the land is devoted to agriculture. More than half of the world’s population live in urban areas. According to the World Health Organisation, there is a higher risk of getting the disease in urban areas than rural areas as it could be considered that those living in the countryside are healthier than those who live in the cities; as in the country side, communities grow their own food which is arguably fresher than having food imported.

Also, the atmosphere could be said to be cleaner as there are more trees and less production companies such as fuels and cars. These production companies produce harmful gases that may contribute to acid rain, “Acid rain causes … toxic metals to be released, they can infiltrate into the drinking water, and the animals or crops that humans use as sources of food. This contaminated food can damage the nerves in children, or result in severe brain damage or even death”. Indeed, Scientists suspect that “aluminium, one of the toxic metals affected by acid rain, is associated with Alzheimer’s disease”.

This research supports the idea that geographical location is a contributing factor of the disease. Interestingly, research has also shown that there are East and West differences when it comes to the rate occurrence of the disease. Studies carried out in South India, Mumbai and the northern state of Haryana in India have reported very low rates of occurrence of Alzheimer’s disease in those of respondents 65 years of age or older, ranging from about 1% in rural north-India (the lowest reported from anywhere in the world where Alzheimer’s disease has been studied systematically) to 2. % in urban Chennai. Also, Studies from China and Taiwan have also shown a lower risk of Alzheimer’s disease compared to western countries. The low rates of occurrence of Alzheimer’s disease in the eastern countries are in striking contrast to data from the western countries. This research supports the idea that living in an urban area may increase the risk of suffering from Alzheimer’s disease. Also, it may seem that those who moved from eastern countries to live in western countries have a higher risk of getting the disease.

Reported research in 1996 among older Japanese Americans living in Washington and in Hawaii revealed that the number of Alzheimer’s disease cases was much higher than that estimated in Japan and closely resembled the findings for North America and Europe. Similarly, research studies were comparing the Yoruba’s living in Ibadan, Nigeria, and African-Americans living in Indianapolis, USA, are also of interest as the groups share an ethnic background but live in widely different environments.

In the Ibadan group, the proportion of Alzheimer’s disease cases was a low 1. 4% (similar to rates in India), while the rate for Alzheimers disease among the African-Americans was estimated at 6. 2%. This research strengthens the argument that geographical location is a contributing factor to the disease. It may seem that developed countries are more at risk of acquiring Alzheimer’s disease and this supports the idea that urban areas have a higher risk of suffering from the disease, suggesting that lifestyle is a contributing factor to Alzheimer’s.

However, there are lower cases of Alzheimers disease in developing countries, and this may not be due to their supposed better lifestyle but this idea may be due to their lack of awareness and knowledge about the disease. Doctors may not be diagnosing the symptoms as Alzheimer’s but as ‘senility’ or ‘old age’ and therefore, the appropriate care is not given to sufferers which can lead to them dying much earlier than if they were supplied with the appropriate drugs. This is mostly common in the African and Asian cultures where they are not medically as advanced.

Not only scientific, but cultural factors are influential when considering the influences of acquiring Alzheimer’s disease. From the literature reviewed, it can be seen that cultural influences can contribute to factors which determine the onset of Alzheimer’s disease. For example, in some cultural groupings, the nature of ‘respect’ is important to consider as unwritten codes of behaviour mean that elders are not forced to take drugs that would alleviate the symptoms of Alzheimer’s. This ideology is common in African and Asian cultures.

It could be argued that the patients are not in their right state of mind to be making such decisions and therefore their word should not be taken into consideration; this questions free will, especially in the argument of patient trialling where authority is given to the family. This strengthens the argument that patient trialling is a contributing factor as to why there is not yet a cure for Alzheimer’s disease. It could be that a lack of education could be a deciding factor as to whether an individual is at risk of suffering from the disease.

According to the World Health Organisation, the majority of studies show that with higher education concerning the disease, there may be lower risk of Alzheimer’s disease. Although, the reason for this association is not yet known, it is possible to suggest that with a lack of awareness of Alzheimer’s disease, individuals are likely to be less cautious of things that can trigger the symptoms of the disease. Also, if there is no knowledge of the disease within a community, then such symptoms of the disease may be linked to old age and therefore dismissed.

This is most common in developing countries, strengthening the argument that geographical location is a contributing factor of Alzheimer’s disease. From the literature reviewed, it is clear that millions of dollars worldwide have been spent the continuous research to determine why Alzheimer’s disease occurs, whether there are possible ways to slow down the symptoms and if a possible generation of a cure can be arrived at. With a lot of money been used every year, the outcomes of each research seem to only suggest are possible triggers, risks and prevention.

But there is never any direct link which is somewhat frustrating to those suffering with the disease, suggesting that there is still a long way to go in research. This weakens the argument that finance is a contributing factor to Alzheimer’s disease. * Heart disease is suggested to be a contributing factor to Alzheimer’s disease as there are findings of a strong relationship between the two conditions. It was shown that “Patients with atrial fibrillation were 44% more likely to develop dementia than patients without the heart disorder”.

Indeed younger patients with atrial fibrillation were at higher risk of developing all types of dementia; particularly Alzheimer’s and atrial fibrillation patients under age 70 were 130% more likely to develop Alzheimers”. It could be argued that diet is a cause of Alzheimer’s disease as eating unhealthy junk food can lead to heart disease. This is more common in urban areas; this supports arguments that lifestyle could also be associated with Alzheimer’s disease. Studies have also shown that taking some vitamins may help prevent the symptoms of the disease, such as: Vitamin D which was seen in low levels in Alzheimer’s patients.

This led to large doses of prescriptions of Vitamin D being prescribed to Alzheimer’s patients and this proved to show them performing better. Hence, it was seen to positively “enhance the amount of important chemicals in your brain and protect brain cells. ” In addition, “Tablets containing high doses of B vitamins and folic acid, reduced memory decline by 70% in some elderly people. It also halved the rate of brain shrinkage in some patients – a physical symptom associated with forgetfulness that can lead to full blown Alzheimer’s disease. This literature strongly suggests that diet could be a contributing factor of Alzheimer’s disease. Also of interest from the research reviewed, coffee is suggested to reduce the risk of Alzheimer’s disease. “Researchers argue that 500 mg of caffeine, or about five cups of regular coffee, is the dose that seems to protect the brain. ” However, this could be seen as an excessive amount and may have other side effects such as dehydration, emotional fatigue and addiction.

Interestingly, this study was tested on Alzheimer’s mice (mice injected with Alzheimer’s human brain tissue into the animal’s brain which will lead to the mice developing Alzheimers over time), showing an improvement in spatial memory, however, as this “research has not yet been translated into findings for humans”; therefore it is not initially reliable to start drinking 5 cups of coffee a day. “A few other smaller studies in Europe have led to similar findings, but experts say the research only establishes a correlation between coffee drinking and brain protection. This research weakens the idea that diet may be a contributing factor to Alzheimer’s disease. Indeed, Reisa Sperling takes this point further by stating, “I’d hesitate to say that there’s epidemiologic evidence that coffee prevents Alzheimer’s disease,” She argues that “Alzheimer’s disease is an incredibly complicated disease. Exercise and good nutrition do seem to be protective, but a person’s risk is largely determined by genes. No one behaviour or diet change — like coffee drinking — can erase that risk”. This research supports the idea that genes and diet are contributing factors to the disease.

People suffering from Alzheimer’s disease are been prescribed drugs to help reduce their symptoms. These drugs are approved by the Food and Drug Administration, however, as the symptoms of Alzheimer’s is different for many patients, certain drugs that help some patients may not help others and therefore there is increased research to arrive at drugs that can meet a variety of patient’s needs and effects. But due to a lack of patients to participate in a drug trial, there is not a use for these new drugs which is somewhat disappointing to those who have done research and developed a drug to help those suffering from the disease.

This suggests that the lack of participants willing to participate in a drug trial is a contributing factor as to why there is yet no cure for the disease. If drugs are not tested then it is not possible to know how they can help or indeed what side effects can result from them which is an issue as families and loved ones of Alzheimer’s patients would not want them to be used for trials in the fear that there could be more damage done to the patient. Another idea from the literature reviewed is whether technology could also be a contributing factor of the isease. Researchers in Sweden argue that using mobile phones, “damage key brain cells and could trigger the early onset of Alzheimer’s disease”. They suggest that being exposed to high levels of radiation which are emitted by mobile phones “damages areas of the brain associated with learning, memory and movement”. However, there is not yet any conclusive evidence to suggest that mobile phones do trigger symptoms of the disease as the study has only been carried out on rats and it is not yet known if the human brain can be affected in this way.

It would seem that this literature is arguing in favour of the reduction of mobile phone usage as the study by Dr. Gary Arendash at the University of South Florida contrasts that of Professor Leif Salford suggesting that mobile phones could protect against Alzheimer’s disease. Once again the study has only been carried out on rats and it is not yet known if the human brain works in the same way. The study was completed on genetically modified mice (introducing desirable traits into animals using recombinant DNA (rDNA) technology) and normal mice.

Interestingly, “The researchers found that the genetically modified mice exposed to high-frequency electromagnetic field from a young age showed less of a decline in some of the memory tasks than those that had not had this exposure. Exposing the normal mice to EMF from a young age had no effect on memory. ” Therefore the research suggests that the exposure to high-frequency electromagnetic field may be more than that received from a mobile phone, so no conclusions have yet to be made.

This supports the idea that technology is a contributing factor of the disease. So it would seem that there are no conclusions that can be made as to what can cause or trigger Alzheimer’s disease. It would seem that every case of the disease is different in each patient and therefore no direct conclusions can be made. The researchers can only produce theories and hypotheses, and it is up to individuals to decide whether to heed the warning signs or indeed reject such research.

There can be no conclusion made if there are no patient trials, which raises the ethical debate about the value of using people as “guinea pigs” for drugs that may not even work for them. Also, with increasing costs of caring for Alzheimer’s patients and further research required in seeking to find a breakthrough, new analysis still seems to be produced but with no direct links to each other. Financially, the burden is huge; “In the US, health care for Alzheimer’s patients will reach $160 billion by 2010 and $189 billion dollars by 2015. Worldwide its $248 billion right at this moment)”. Indeed, It could be argued that the government should resource further research into a possible cure, however, should the government resource a “bottomless pit” into research and care homes facilities for sufferers as a cure has yet to be found and resources could be best put elsewhere such as research into cancer. This suggests that costs are a contributing factor as to why there is not yet a cure for the disease.

There could be possible hopes for those who are worried about being victims of this “mind-robbing” disease, as UK scientists suggest that a simple eye test might be able to detect Alzheimer’s and other diseases before their symptoms develop. Indeed, “Fluorescent markers attach to dying cells and can be seen in the retina which can give an early detection of brain cell death,”which can be used to track the progress of the brain.

However, Patient trials are in their formative stages as research has only been done on mice and so it could be possible in the future that eye tests can also be tests on the state of our brain and we would no longer be worried about the disease. The journey to discover a cure is still one that is ongoing and considered by scientists as a worthy venture to investigate. DISCUSSION In response to the research question, why is there no cure for Alzheimer’s disease? It is clear from the evidence research that there could be a cure for Alzheimer’s disease if proper funding and appropriate research is in place.

Appropriate research being that which has shown a big difference in the symptoms of the disease, for example, the use of an anti-inflammatory drug called Perispinal Etanercept initially trialled and designed to treat rheumatoid arthritis (a condition in which the lining of the joints become inflamed). However, Dr. Edward Tobinick used the Perispinal Etanercept drug to target a protein called TNF that is present in all humans but 25 times higher in patients with Alzheimer’s disease.

TNF influences inflammation in the brain, and by damping down the process, arguably, it has the ability to preserve brain function. The drug “worked within minutes” evident from video footages of trial patients. Professor Edward Tobinick, who led the research, said “What we see is an improvement in ability to think and calculate, memory improves, verbal ability improves, [patients] find words easier, they seem happier and we often also see an improvement in gait in patients whose gait is affected. This suggests that the Perispinal Etanercept drug was effective and could possibly be a ‘breakthrough’. However, this drug has been criticised for not going through rigorous trial stages, instead the drug has been promoted to the public; this raises concerns about the ethics of the trial process and the safety to prospective patients. Although, the results of the drug may be fascinating, criticisms of the drug are that it should have gone through randomized controlled trialling so the field can interpret the data.

This is important so that the drug can be observed for any side effects and similarities with other drugs. The lack of a trial undermines the importance of drug trials for finding a cure for Alzheimer’s disease because the difficulty for such trials relies on patients coming forward to participate. There have been ethical issues as to whether people should be used as ‘guinea pigs’, therefore, many families are not willing to approve of their loved ones participating.

An argument for skipping the drug trial stage could be that it allows for treatment to be responsive to an individual’s view. However, this means that National Health Societies and Insurance may not cover the costs of taking the drug, and as the positive effects of the drug relies on it being continuously taken, some people may struggle to afford the drug, especially if there is a dramatic improvement in the sufferer. This research suggests that the lack of patient trialling is a setback in the journey to finding a cure for Alzheimer’s disease.

Age is a contributing factor to the disease, Dr. Dharma Singh Kalsa reports that “Last year, over 500,000 people younger than 65 were diagnosed with Alzheimer’s — some of them in their 20’s and 30’s”, however, the extent to which an individual should really start to worry during their 20’s to 30’s is questionable. Martha Weinman Lear argues that “with normal ageing, what we lose is not memory in general but a particular kind”. By this, she means that it is only a part of an individual’s memory that is lost as “We have many kinds. An example is the“procedural memory, which is how-to-walk, how-to-eat, how-to-tie-a-shoe memory”. This memory without thinking about it comes naturally and it is the strongest type individual’s have. A second is “semantic memory, which covers facts suchas what is a key? What are eyeglasses? What is a movie? ”This is the memory for understanding the meaning of things. And a third is “episodic memory, which covers experience such as I’ve lost my keys. Where did I leave my glasses?

Who was in that movie? This is the recall of specific events and experiences; this is the most affected memory when suffering from Alzheimer’s disease as the episodic memory relies heavily on the frontal lobes- front areas of the brain which are the first to start shrinking. All of these features suggest that with time, the “100 billion neurons” a person has in their brain which send electrical and chemical signals around the body to make memories, will weaken, this causes the brain to shrink about half a percent a year, starting around the age of 30, but these shrinkages would not be noticed for years.

Lear also argues that “We actually may be wired to forget. ” By this she means that if everything is stuck to what she refers to as the ‘mental flypaper’ then the brain will be overwhelmed with irrelevant information. The longer we live, the more memories we have, and the harder it may become to locate any particular one. So those that we need least, the episodic memories, get stored in the ‘attic’ first. There is no importance in remembering the restaurant you ate at last night as it does not help a person survive in the world. This suggests that forgetfulness is a natural process of ageing.

What the symptoms of Alzheimer’s disease suggests is that behaviour’s will be categorized by how intact our ‘procedural memory and semantic memory’ are, as these help a person survive in the world by determining what is eating and how to eat. It is clear therefore that age is a contributing factor to Alzheimer’s disease but individuals do not have to start to worry about it in their 20s and 30s. Gender is considered to be a contributing factor to the disease with women being most at risk than men. Personally, I would not consider gender to be a contributing factor as the disease affects the brain.

Men and women have different brain sizes, it does not matter how intelligent a person is, they could still become a victim of the disease. However, women are argued to be more likely to develop Alzheimer’s disease than men because “One factor that has been suggested in the development of Alzheimer’s disease is a lack of the hormone oestrogen in women after the menopause. ” This suggests that women with low levels of oestrogen are more likely to acquire Alzheimer’s disease as it influences and modulates brain structure and function.

The use of Hormone replacement therapy (HRT) is considered as a possible prevention of Alzheimer’s disease, however, controlled studies have suggested that HRT has “no beneficial effect on the development of Alzheimer’s disease, and may even increase a person’s risk of developing the condition”. However, a weakness is that there is no evidence to support this conclusion so it is not recommended that women take HRT as a way to reduce their risk of developing dementia.

This research suggests that the lack of finance for appropriate research is a setback for finding a cure for Alzheimer’s disease. Lifestyle is one of the most important contributing factors of Alzheimer’s disease. Having a healthy and balanced diet with regular exercise can enable an individual to maintain a normal body weight, this results in lower risks of developing high blood pressure which can lead to heart disease which “puts a person at a greater risk of developing dementia”.

This is because saturated fat causes a build-up of fatty substances in the arteries causing them to become narrow, this reduces blood flow to the heart tissue and so less oxygen, glucose and nutrients reach the heart leading to a higher risk of developing ‘heart attacks, stoke and vascular dementia’. Regular exercise helps to keep the body system healthy, it helps protect against many conditions, including vascular dementia. Fresh fruit and vegetables contain many vitamins and antioxidants, which may prevent heart disease and protect the brain.

A number of research studies have shown that the polyunsaturated fatty acids found in oily fish might also help to protect the heart and blood vessels and lower the risk of developing dementia. However, as Alzheimer’s disease is transferrable by genes then this increases a person’s chance of acquiring the disease even if they do live a healthy lifestyle. Smoking is also very harmful to the heart and can also result in vascular dementia, despite earlier studies suggesting that smoking might cause a reduced risk for Alzheimer’s disease.

However, more recent epidemiological research has shown that smoking is a significant risk factor for Alzheimer’s disease and is ‘twice more likely to develop in smokers than non-smokers’. This research supports the argument that lifestyle is a contributing factor to Alzheimer’s disease. Taking supplements such as Vitamin D, drinking caffeinated coffee and living a healthy lifestyle can reduce chances of acquiring the disease.

This support the argument that living in urban areas and moving to western countries means there is a higher risk of getting the disease as these areas are more modernised and could be argued to promote an unhealthy lifestyle with high development rates and increasing growth in population. This means that agriculture is moved aside for modernisation, causing also an increase in pollution and therefore increasing the risk of individuals suffering from Alzheimer’s disease. This also supports the idea that developed countries have a higher risk of suffering from the disease.

Supportingly, Guy Eakin PhD reports that “as countries grow economically and the average lifespan of their citizen’s increases, more people are at risk for this disease and other forms of dementia. ” This suggests that there is a necessity to work towards a cure as with an increasing population then there a higher risk of acquiring the disease. The government thereby needs to provide more finance for the development of research in order to educate its population about the risks of the disease, without ‘enough’ finance the government are at risk of a ‘growing problem’.

This suggests that the role of the government is a setback in acquiring a cure for Alzheimer’s disease. I do not believe that lack of education is a contributing factor to Alzheimer’s disease, as surely not knowing about the disease does not necessarily mean a person will have a higher risk of contracting the disease. In contrast, lack of awareness is most common in developing countries, which have been found to be less at risk due to their lack of modernisation and increase in agriculture, meaning that it is argued that they live a healthier lifestyle, free from pollution.

In contrast, Bill Hendrick reports that “Having more education reduces the risk of Alzheimer’s disease but does not slow memory loss once it starts, says a new study”. This suggests that being ‘smarter’ does not change scientific issues but it does mean that a person is more aware of the risks of the disease and could be able to discontinue behaviours that increase the risk of acquiring the disease. However, the government are still responsible for educating the population about the risks of the disease and without this being done, there still remains a higher risk of acquiring the disease.

Additionally, the study investigated by Robert S. Wilson, PhD, with the Alzheimer’s disease Center at Rush University Medical Centre in Chicago concluded that “… education is robustly associated with level of cognitive function, but not with rate of cognitive decline. ” This supports my view that having higher education does not mean there is less risk of having the disease. In contrast, Dr Nikolaos Scarmeas argues that “Overall mental agility declined every year among all the patients, but each additional year of education equated to an additional 0. 3 per cent deterioration. This suggests that having a higher education may reduce chances of developing the disease because their brains “develop the decreased mental agility of Alzheimer’s disease for later because can tolerate changes for longer”. This opposes my view that education is not a contributing factor to contracting Alzheimer’s disease. I do not believe that the right amount of funding has been put into research for Alzheimer’s disease. It could be argued that most governments do not believe that a cure can be derived from all the research been done at present, with the disease been referred to as a “bottomless pit”.

I do not think that should therefore decrease the funding for the research, as there have been proven links and suitable research for more links needs to be continued. Guy Eakin PhD argues that “The greatest threat to research advancement is the inadequate financial support available to researchers. There’s just not enough research funding to support the number of promising scientific projects, particularly in this era of government cut-backs”. Funds will always be constrained but if Alzheimer’s disease is not prioritised then no progress will be made.

With an ageing population, there is an increased chance of individuals acquiring the disease; the governments may end up having to spend more money for care facilities in the future and may be forced to put in ‘enough’ funding for ‘promising scientific projects’. This supports my view that a lack of funding is a setback in finding a cure for Alzheimer’s disease. Among the top 10 deadliest diseases in the U. S. , “Alzheimer’s is the only one with no treatment to slow or stop the disease. ” With cut-backs due to downgrading economy, funding for Alzheimer’s disease is even further behind.

Unlike the other diseases categorised as the as the top deadliest in the U. S. , if you have Alzheimer’s disease, you will end up dying from it because there is yet no cure. The government fail to prioritise, awarding ‘several billions of dollars to heart disease and cancer’, all with effective treatments and cures. In contrast, the government awarded only “$450 million for Alzheimer’s disease, despite the demographic wave of people facing Alzheimer’s over the next three decades, numbers that could bankrupt the health system. This supports the argument that lack of finance is a setback for finding a cure for Alzheimer’s disease.

In Support, Dr. Marilyn Albert, (director of the Johns Hopkins Alzheimer’s disease Research Centre) argues that “I don’t think there is anybody involved in Alzheimer’s research who thinks these major government agencies are spending enough on Alzheimer’s disease care and research”. At present, about ‘$6 billion a year’ is allocated to cancer research, while Alzheimer’s receives about ‘$500 million to $600 million a year. She argues that there is not enough funding been given to further research for a possible cure for the disease and that ‘increasing Alzheimer’s disease funding to a minimum of $1 billion annually; would be an adequate sum. ’ I support this view, as with the ‘ageing population’, an increase in finance is imperative. The symptoms in many patients may differ, but scientists have been able to narrow down the most occurring symptoms and produce drugs suitable for them. Drugs such as: Namenda, Razadyne Exelon and Aricept.

However, “These drugs’s main effect is to delay progression of some of the symptoms of moderate to severe Alzheimer’ s. ” This means that sufferers are able to perform some daily functions ‘a little longer than they would without medication’. In contrast, Guy Eakin PhD argues that “To date, the few existing treatments for Alzheimer’s disease minimize some of the symptoms and delay the loss of memory in some cases, but without slowing the underlying damage to the brain. This suggests that the drugs at present are not really helping to possibly cure Alzheimer’s disease, they are just relieving the symptoms. For some people, if a loved one is able to regain some of their memory, there would be appraisal OF the drugs being prescribed to sufferers at present. However, the anti-inflammatory drug called Perispinal Etanercept which showed an outstanding progress in memory gain may be able to prove otherwise if it undergoes the trial stages as well as the government financing its production and distribution to sufferers.

This supports the argument that patient trialling and insufficient finance is a setback to finding a cure for Alzheimer’s disease. This leads to my viewpoint on patient trialling, it may seem unfair to want to use a patient as a “guinea pig” to trial a new drug, however, I believe that such trialling is beneficial because scientists interpret the data and understand the side effects of drugs especially with the increasing rates of the disease and there not being an available cure yet. I believe that being able to test these drugs can help bring the world closer to finding a cure. Dr. Howard Chertkow (one of Canada’s leading Alzheimer’s clinician), argues that “up to 20 years before a diagnosis, neuron damage is occurring in the brain, from protein misfolding, inflammation and cellular oxidation. ” He suggests this as a possible reason for the failure of drug trials; he argues that “researchers are enrolling patients too late in the disease process. ” This weakens the argument that individuals should not be concerned in their 20’s and 30’s; if the disease starts developing at an earlier stage then surely the government should be financing research into brain activity from the age of 20.

This supports my view of there not been sufficient finance into researches concerning a possible cure for Alzheimer’s disease; which is somewhat frustrating to those who are doing the research for a possible cure. For example, the anti-inflammatory drug called Perispinal Etanercept which was described as “the breakthrough drug” for Alzheimer’s disease showing “dramatic improvement” in the sufferer was criticised for not having been tested appropriately: “no controls, placebos or test to show the drugs real effect and a response so rapid that most TNF mechanisms could not be involved.

It would have to be an immediate immuno-neutralization and signal transduction effect. ” Cynthia Lemere, (associate professor of Neurology at Brigham and Women’s Hospital in Boston) asserts “This is exciting but very preliminary information,” She argues further that “The appropriate way to pursue it at this stage is to apply to FDA and NIH for support to run a rigorous trial, not to promote it to the general public. The consequence of not having patient trials is that the drugs cannot be supported by the National Health Service meaning that such drugs are administered privately and rely upon each individual financing the scheme. This makes it difficult for most sufferers to be able to benefit from the positive “dramatic changes” of the drug. This supports my view that patient trialling is essential to help find a possible core for Alzheimer’s disease and further supports the argument that a lack of patient trialling and sufficient finance is a setback to finding a cure for Alzheimer’s disease.

In answering the question, why is there no cure for Alzheimer’s disease? My discussion arrived at lack of finance being the major setback. Without finance, then sufficient research, awareness and investigation cannot be carried out. Without enough supporting research into a drug or its risk factors, then individuals become sceptical about believing in the drug. This leads to individuals being sceptical about being used as a ‘guinea pig’ in patient trialling, causing drugs to not be properly analysed and evaluated.

Governments believe that the ‘journey’ to finding a possible cure is too long and are refusing to provide more finance for this ‘bottomless pit’. However, the ageing population is increasing, chances of acquiring the disease are also increasing; I believe that it is time for the government to prioritise Alzheimer’s disease by putting in more funding for research into finding a possible cure for Alzheimer’s disease. CONCLUSION AND EVALUATION

Originally, my viewpoint on Alzheimer’s disease was very pessimistic because scientists have been researching into a possible cure since the first case of Alzheimer in 1901, so for about 111 years there has not yet been a cure found, or even an efficient drug for managing the disease. Through research I have found that a major reason why a cure is yet to be discovered is because we do not know what causes Alzheimer’s disease. There have been factual links to the cause of Alzheimer’s disease such as Age and Genes, to hypotheses on what are contributing factors of the disease; such as Diet, Lifestyle, Education and Gender.

Not being able to find out what causes the disease is leading to ongoing researches and new research being carried out. However, with a lack of a breakthrough on any of the research carried out, I think governments are sceptical about increasing funding for further research into links and possible cures. However, with the ageing population and Alzheimer’s disease cases predicted to ‘double’ by 2025, I feel that Alzheimer’s disease has to be prioritised and more funding should be provided for research.

I also think that a major setback is the lack of patient trialling; therefore people should be willing to participate so as to be able to interpret data on the drugs and be observed for side effects. After completing the project, I am optimistic about finding a possible cure for Alzheimer’s disease because there is a ‘breakthrough’ drug been offered to patients called Perispinal Etanercept which has shown ‘extraordinary improvements’ in patients.

I feel that if this drug is properly researched and trialled with the right funding then we could be looking at ‘the cure’ for Alzheimer’s disease. Whilst carrying out my research, I found that Perispinal Etanercept has not undergone any research or patient trialling but yet seems to be very effective, so I think it would be interesting to investigate further on how the drug affects patients with Alzheimer’s disease.

Throughout working on this project, I have developed scientific knowledge into how the brain works and the importance of keeping your brain healthy, through our lifestyle and geographical location. From researching into opposing and supporting views, I have learnt how to distinguish between reliability, validity, trustworthiness and biased sources; this has helped by critical thinking and my ability to analyse and evaluate sources, giving me a broader perspective on the subject.

Cite this Why Is There No Cure for Alzheimer’s Disease?

Why Is There No Cure for Alzheimer’s Disease?. (2017, Jan 28). Retrieved from https://graduateway.com/why-is-there-no-cure-for-alzheimers-disease/

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