Category: Alzheimer’s Disease

Alzheimer’s disease is a serious condition affecting the lives of millions of people. Its symptoms and consequences worsen with age. The disease can be caused by numerous factors, and cannot be cured. This paper will provide the background information on the possible reasons leading to the development of this condition and possible ways of preventing it.

Alzheimer’s disease is characterized by “a gradual decline in memory and other cognitive functions and neuropathologically by gross atrophy of the brain and the accumulation of extracellular amyloid plaques and intracellular neurofibrillary tangles” (Karch et al. 11). In simple words, it is the condition caused by the negative changes in the human brain that, as the end result, leads to memory loss and some behavioral issues that worsen the quality of patient’s life. Among other primary symptoms, there are initial memory lapses that later evolve into losing things around the house, facing difficulties in expressing one’s thoughts, e.g., problems with finding the necessary word, concerns with forgetting recent events, hardships in making decision, judging situations or with sequential tasks, losing orientation etc. (“What is Alzheimer’s disease” par. 9, 11).

This condition has a robust genetic component behind it, as it has been proved that mutational in genes are the ordinary cause of the disease. What should be stressed on about the genetic background of the disease is that these are the mutations in proteins that lead to its development, namely amyloid precursor protein (Karch et al. 11).

Except for genetic aspects of the disease, there are is also a strong environmental component that adds to it. What is meant by the word environmental is not only what surrounds the patient but also the way of life he/she leads and the habits he/she has. For this reason, they can be divided into two groups – solely environmental and so-called habitual.

As of the first group of causes leading to Alzheimer’s disease, it includes exposure to pesticides and toxins and electromagnetic fields and high aluminum intake with water. Speaking of the lifestyle habits that may provoke the disease, they are little physical exercises, excess consumption of alcohol, imbalanced diet often resulting in obesity, etc. There are also some external factors that have to do with the state of health but cannot be controlled by those in the risk group, for example, diabetes, inflammation processes, high blood pressure, and serious head traumas (Campdelacreu 541).

Unfortunately, nowadays, there is no cure to Alzheimer’s. That means that nobody can be absolutely safe from it. However, there are some basic steps that can help prevent the development and worsening of the diseases. The primary prevention tool of the Alzheimer’s disease is leading a healthy way of life including enough physical exercise, balanced diet, and cognitive activities. What is also of crucial importance is enough mental activities and social interactions. In the case if the patient knows that he/she is in the risk group, the decision to fight possible inflammations, the formation of neurofibrillary tangles and further protein mutations can be made (DeKosky 14).

That said, Alzheimer’s disease is a serious illness caused by a wide range of factors. It is the condition that cannot be controlled or cured once it started evolving but it can be prevented or slowed down by following a simple set of recommendations centering on enough physical and mental activities and balanced diet.

Works Cited

Campdelacreu, Jaume. “Parkinson’s Disease and Alzheimer Disease: Environmental Risk Factors.” Neurologia 29.9 (2014): 541-549. Print.

DeKosky, Steven T. Alzheimer’s Disease: Current and Future Therapies. 2014. Web.

Karch, Celeste M., Carlos Cruchaga, and Alison M. Goate. “Alzheimer’s Disease Genetics: From the Bench to the Clinic.” Neuron 83.1 (2014): 11-26. Print.

What Is Alzheimer’s Disease. n.d. Web.

Introduction

The target population is the older generation. This is because scientific studies have demonstrated that the risk of developing the disease is positively correlated with age. The disease is highly prevalent among the older generation and has a great impact on quality of life that individual life and it further places so many demands on the healthcare system due to care involved in managing the patients.

Population Demographics

It is estimated that about 3% of men and women aged between 65 years and 74 years have Alzheimer’s disease and over 50% of the population over the age of 85 have the disease. At least one person out of ten people over 65 years has Alzheimer according to ADEAR. It is pertinent to note that having Alzheimer’s disease in old age is not part of the normal process of aging (Administration on Aging, 2003, p. 3). This is just the commonest dementia among older people.

Currently, the disease affects 5.3 million people of older population and slightly over 50% of them are receive their care from home while the rest are in different healthcare facilities across the country. Most of the Alzheimer’s patients are ages 65 years and above, though some patients can develop the disease early as in their 30’s (Administration on Aging, 2003, p. 3).

After the 65 years, it has been found that the probability of developing Alzheimer’s disease doubles after every 5 years and as a result, by the age of 85 years, the risk of acquiring the diseases is about 50%. According to Alzheimer’s disease, the prevalence of the disease is expected to rise to between 12 and 16 million cases by 2050 in America (Sloane et al, 2002, p. 213).

General Impact of Changing Demographics on Health Market

With the number of older population having a steady rise because of improved healthcare system, many American get live up to the life expectancy of 70 years (Hebert et al, 1995, 1356). This has made AD to become number six on the leading causes of deaths in America today. It’s expected that this trend with reach 1 million new cases of the disease per year by 2050.

The healthcare expenses are expected to increase considerably (three-fold) per person, for AD sufferers as well all patients of other dementias compared to other older people without this health condition (Administration on Aging, 2003, p. 4). The Medicaid payment has risen to nine times higher in 2050.

The out-of-pocket expenses have increased to 28% higher for the AD patient population that benefits from Medicare than those without the disease. Those patients who received health care from home record the highest expenses of up to an average of $16,689 per year.

These numbers underscore the potential increase in the US medical burden care burden. There is likely to be a knock-on impact with cost related to management of the disease especially the cost of drugs and hospital care services. These projections may draw federal government involvement, resulting into an initiative for AD that would address provision of extra care for the patients (Brookmeyer et al, 1998, p. 1339).

The numbers also indicate that the AD drug will increase in the market to cater for the growing numbers. So far, this sector has had high-value treatments that have the pursuit of pharmaceutical companies. The prediction of increase cases and cost includes drugs costs hence an opportunities for drug manufacturing firms (Brookmeyer et al, 1998, p. 1339). By 2009, the AD drug market had reached $5 billion.

Key challenges

The main challenge is the cost of care. In most cases AD can last for longs as it’s a chronic condition. Medicare does not pay for these longer healthcare services. It is only for the short-term cases that the Medicare advantage pays for the stay in a health facility (Brookmeyer et al, 1998, p. 1339). Medicare pays only for the first 20 days of stay and when the patient stays for more than these 20 days, the patient has to co-pays the balance of the days.

The second challenge is the prescription medication costs. Medicare usually pays for all the medications that are administered when the patient is admitted in the hospital of any health facility even when they are not AD patient. Medications that are given in the doctor’s office are also covered by the part B provision of Medicare (Sloane et al, 2002, p. 213).

However prescription drugs taken at home are a great challenge. The part D of Medicare provision only covers specific drugs prescribed for AD but still, that would depend on formulary – list of the covered drugs.

Market Needs for AD

The current medications are very costly and this has lead to poor adherences to medication as the patients or their families cannot afford these drugs. Medicare only pays for the drugs given in hospitals and a certain number of drugs for home prescription. This means that pharmaceutical have to develop cheaper alternatives to supplements the current drugs in the market (Brookmeyer et al, 1998, p. 1342).

Alternatively the government should step in and subsidized AD drugs to make them affordable. Moreover, the soaring numbers makes these drugs highly on demand hence the cost increased due to demand dynamics (Hebert et al, 2003, P. 1121).

The healthcare setting is very expensive while the current system is only appropriate for handling acute cases; this makes chronic care a challenge. It seems to disregard that the needs of AD patients require chronic care services, quality service, cost-effective and provide social support (Hebert et al, 2003, P. 1121).

AD patients can be best cared for at home, however, the current programs do not provide adequate funding for ensuring there is safety and proper welfare of AD patients is socially support setting (Brookmeyer et al, 1998, p. 1342). Furthermore, there are very limited alternatives to offer AD patient the psychological and social stimulation needed for symptoms management and slowing disease progression.

Chronic Wellness Program

Considering that AD is a chronic and degenerative medical condition, a chronic wellness program would be very appropriate for handling the disease (Sloane et al, 2002, p. 211). This will allow access to educational support, and care providers will be able to learn best practice, identify products and services to enhance in-home care and allow patient to be serviced by professional care givers who are well conversant with the disease challenges (Hebert et al, 2003, p. 1122).

Individual and Community Support

With the escalating cases of the diseases are portrayed by the demographics, Medicare alone cannot be able to deal within the needs of these patients. Besides, over 70% of the AD patients depend on their families for daily care and the condition has extraordinary financial and emotional burden on the care providers (Meagher et al, 2009, p. 86). This therefore means that all the stakeholders must get involved, from individual patient to the society at large. This is a holistic approach to handle the problem and requires collective effort.

The combined effort would therefore include identification of mutual interests, development of new relationships and forming partnership to pursue these interests (Meagher et al, 2009, p. 86). This will form a network where individuals help in expansion of the objective and the impact of the collective responsibilities for the diseases. The goal should not be anything leas that finding the best cure and management strategy and making it accessible to all those in need of it (Meagher et al, 2009, p. 89).

Reference List

Administration On Aging, (2003). Statistics On The Aging Population. Rockville, MD: US Department Of Health And Human Services; U.S. Bureau Of The Census

Brookmeyer, R., Gray, S., & Kawas, S. (1998). Projections Of Alzheimer’s Disease In The United States And The Public Health Impact Of Delaying Disease Onset. Am J Publ Health, 88,1337–1342.

Hebert, L. E., et al., (1995). Age-Specific Incidence Of Alzheimer’s Disease In A Community Population. Jama 273:1354-59.

Hebert, L.E, et al, (2003). Alzheimer Disease In The US Population: Prevalence Estimates Using The 2000 Census. Arch Neurol; 60:1119–1122.

Meagher, B., Penfield, S., & Lee, R. (2009). Commentary On “A Roadmap For The Prevention Of Dementia II: Leon Thal Symposium 2008. The Megacommunity Approach To Alzheimer’s Disease. Alzheimer’s Dement. 5 (2), 85-92

Sloane P. D., et al. (2002). The Public Health Impact Of Alzheimer’s Disease, 2000–2050: Potential Implication Of Treatment Advances. Annu Rev Publ Health, 23, 213–231

Summary

Dementia is an ailment that occurs mainly as a result of brain malfunctioning. In turn, memory shortage is likely to occur due to aging. However, excessive memory loss is not a normal situation and leads to Alzheimer’s disease.

Besides, Alzheimer’s disease remains the most frequent illness suffered by many people in their old ages. In most cases, when Alzheimer’s disease occurs the brain is affected first since the patient tends to suffer from loss of memory. However, the chances of the disease occurring can be reduced by preventing the risk factors.

Observing health matters is a requirement to help prevent the disease. In fact, keeping fit by engaging in physical exercises may help keep the patient’s brain relaxed and fresh. Feeding habits alongside diets should also be put into consideration. People suffering from the disease should eat food rich in iron, vitamins, and maintain healthy diets. The article recommends that spices should be used when cooking food for people suffering from Alzheimer’s. Patients must remain focused on realizing their life missions.

Besides, emotional support from close people like family members is healthy to help support a person suffering from dementia. Such support reduces the chances of being stressed, which may eventually lead to Alzheimer’s disease. The mind is also supposed to be put to rest to avoid straining. Once diagnosed with Alzheimer’s disease, the use of drugs such as alcohol and cigarettes should be avoided. A habit that subjects the heart to risks like smoking also subjects a person to the risk of getting Alzheimer’s.

Relating the article to personal experiences

A digital sabbatical is taking rest from the internet and all its applications. It is a time for one to clean the mind and take time to do what matters most in life. The sabbatical also helps one to stop being dependent on the internet. Despite the fact that the internet and computers are important for learning and communication, they need to be used wisely. A digital sabbatical in the house is very important. It gives you time to relax, think, and meditate as well as offers space for self-reflection.

People with dementia are better handled, naturally and digitally. While engaging them in physical activities to keep them healthy, dementia patients should also be encouraged to have a lot of rest. With an increased level of technological advancements, a digital sabbatical is mandatory to lower the level of Alzheimer’s disease. To help patients recall past events and people, engaging them in artworks such as sketching assists in distracting their minds and enable them to interact and express themselves.

When fatigue and dis-contentment set in a patient’s life, the person just wants to relax, learn new things or spend more time with his or her families. In fact, during this time, one just feels like going back to the past when life was simple with the limited rush to be online. Instituting a digital sabbatical would be a great way to escape the current era of technology that increases the level of Alzheimer’s illness.

A study conducted by Alexander and Larson (2014) indicated that lifestyles such physical activity, social connections, and constant mental engagement had increased the possibility of reducing incidences of AD. The main challenge of being digital is that it limits movements. Limited movements result in various health problem such as obesity. During a digital sabbatical, it will be an opportunity for movement, which helps in keeping the brain active for longer hours and facilitate blood circulation.

One can exercise at this time given that physical activities do not require electronics. During such times, the patient could visit old friends and relatives to have a conversation with them. Besides, a digital sabbatical would be a great opportunity to go camping or fishing and even find your purpose in life. Therefore, a digital sabbatical promotes a healthy lifestyle and reduces the chances of suffering from Alzheimer’s illness.

References

Alexander, M. & Larson, (2014). Patient information: Dementia (including Alzheimer’s disease) (beyond the basics). JAMA, 38(4), 302-341.

Alzheimer is a mental complication that results from progressive impairment of the memory (Small, Rabins & Barry, 1997). This complication results into difficulties in communication, ability to recall as well as personality and behavioral related disorders. In most cases, these difficulties are used for diagnosing the disease.

There are several factors such as aging, heredity, blood pressure and head trauma that may make an individual to be susceptible to the illness. Research evidences illustrate that Alzheimer has no specific cure. Nevertheless, there are measures that can be taken to control and manage the symptoms.

These include cognitive, pharmacological and other alternative control measures. This paper seeks to compare and contrast the three therapeutic interventions on the basis of their effectiveness, validity, efficacy, symptom, behavior management and recidivism.

It is apparent that pharmacological treatment is widely used to treat Alzheimer. Nonetheless, researchers recommend that non-pharmacological therapies should be tried first. Natural therapy entails numerous treatments such as aroma therapy, dieting and taking mineral supplements such as vitamins (Cummings, Frank & Cherry, 2002).

This implies that cognitive and natural therapies are highly perceived to be effective as opposed to pharmacological treatments. It is on this ground that these non pharmacological therapies are considered to be more varied since they are both ancient and traditional. Research has shown that the level of efficacy obtained in both cognitive and natural therapy is very promising.

Multiple studies have thus shown that these therapeutic measures are highly beneficial and reliable to treat Alzheimer than the pharmacological measures. Moreover, random surveys have shown that their efficacy level is widely recognized by both patients and healthcare providers. Therefore one cannot deny the fact that cognitive and natural therapies have high level of recidivism as opposed to pharmacological treatment.

One cannot ignore the fact that both cognitive and natural therapies have become widely accepted in treating identified signs and symptoms of Alzheimer as opposed to pharmacological therapy. It is also imperative to note that symptoms such as personality problems, delusions, agitation, mood disorder and aggression may not be treated by medications.

Instead, it is cost effective to apply cognitive and natural therapy to manipulate abnormal signs that are associated with behavior and personality. Health providers highly recommend that cognitive and natural therapies are very essential in managing behavior as opposed to pharmacological therapy. This is based on the fact that behavior can not be treated. Instead, it can be manipulated to the desired manner.

However, despite the fact that cognitive and natural methods are highly effective, to some extent, they are unable to control common non-cognitive/natural symptoms such as constipation, irritation and other physical illnesses. For this case, non-behavioral symptoms prompt individuals to use pharmacological interventions in order to treat the disease (Small, Rabins & Barry, 1997).

It is evident that despite the huge contrasts that exist between pharmacological and non-pharmacological therapies, they have slight differences. For instance, research has shown that the efficacy rate is almost the same. Clinical trials have shown that all the measures have equal placebo in terms of response frequency. This implies that patients respond to the measures relatively the same manner.

For instance, study has shown that miss-application of such therapeutic measures can be problematic to patients. Moreover, evidence has shown that there is no specific treatment that is appropriate on its own. In this case, prescription of a single method only might trigger substantial effects that might be harmful to the patients’ health (Cummings, Frank & Cherry, 2002).

Besides, all the treatment measures have common side effects such as falls and sedation. Nevertheless, it is imperative to note that the side effects for pharmacological therapy have more adverse effects on patients’ health as opposed to the other treatment measures. Finally applications of such methods require adequate clinical knowledge in order for one to be able to manage behavior and the indentified symptoms.

References

Cummings, L., Frank, C. & Cherry, D. (2002). Guidelines for managing Alzheimer’s disease: part II treatment. Am Fam Physician. 65, 2525-2534.

Small, W., Rabins, V. & Barry, P. (1997). Diagnosis and treatment of Alzheimer disease and related disorders. Consensus statement of the

American Association for Geriatric Psychiatry, the Alzheimer’s Association, and the American Geriatrics Society. JAMA, 278, 1363-1371.

Alzheimer disease is a form of dementia which grows severely as it progresses. It is a fatal disease which was named after Alois Alzheimer. The latter was the first scientist who explored and fully described the existence of the disease among human beings (Brill 34).

The ailment usually develops with multiple symptoms that may be easily confused with those of other similar or closely related complications. The most remarkable feature of the disease is the loss of ability to remember events in an individual’s life. Thinking abilities of patients are significantly compromised.

As a result, it becomes quite cumbersome for them to maintain a regular mental sequence. It is also worth to mention that the malady advances with more evident symptoms such as total memory loss, confusion and irritability (Green 90). The affected persons begin to move away from family members and they also develop some kind of aggressive and repulsive behavior which makes it difficult to control them.

The most specific causes of this condition have not been fully established in the past medical records and diagnoses. The most reliable sources argue out that the disease is caused by tangles and plague in the brain (Harris 102). The two factors are yet to be studied in detail in terms of whether they are indeed responsible for this kind of ill-health or not.

Currently, there are still wide array of opportunities through which more specialized studies can be undertaken to examine the etiology, prevalence, treatment and cure of the disease. It is true that there is no particular cure for this disease.

It has proven to be quite difficult to reverse its occurrence which usually culminates into full blown Alzheimer (Lau and Berg 163). It is worth noting that exercises conducted with the aim of stimulating the mind remain as a major way of helping victims. It is clear that patients have to depend on the care of others.

As pointed out earlier, the exact cause of Alzheimer is not clear yet. There are many hypotheses which have been put across in an attempt to explore dominant cause or causes of Alzheimer. It is important to look in to each of these studies in a bid to come up with a significant and conclusive understanding of the condition.

The oldest known hypothesis that attempted to examine the cause of Alzheimer claim is that of the neurotransmitter agent in neurons (Warner 198). The latter explains that a problem in acetylcholine which is the neurotransmitter between neuron synapses is responsible for breakdowns towards the smooth flow of communication. This condition has not been able to receive any amicable repair and hence remains a protracted medical and health challenge (Warner 123).

Another hypothesis on the etiology of this disease is that which relates amyloids to Alzheimer. According to the latter hypothetical medical study, it has been exemplified that the presence of deposits of amyloidal cells is the major cause of Alzheimer.

This postulation is equally supported by the fact that amyloidal deposits lead to the creation of excess gene copies (Brill 78). Some of the genes include the mutant and trilogy communication genes which often cause plagues right inside the brain. Oxidative stress is also linked with the perpetration of dementia.

This creates a path for the pathogenesis of the disease. Loss of brain cells has also been associated with the condition (Green 218). Degeneration of glial cells (brain cells) also culminates into increase in chances of the disease condition. This might be as a result of faulty phagocytosis or accumulation of bi products of oxidation. The latter products are largely considered to be toxic to the brain and may cause long term health complications.

The diagnosis of Alzheimer

This disease is diagnosed by following the history of victims in terms of their past health records. It may entail all clinical observations of relatives of the identified patient. This is normally aimed at noticing any features which may be a proof of the disease. The screening techniques used in this case help in identifying all traces of malfunctioning cells in the brain (Harris 68).

Moreover, cerebral scans help in auditing all cases of impairments as well as cognition abilities. On top of this, the intellectual functioning of an individual is also assessed. In most cases, the occurrence of a total diagnosis is only possible during post mortem activities. This is useful in standardizing the procedures of diagnosis (Lau and Berg 203).

The World Health Organization (WHO) has been able to give clear guidelines on how this malady can be identified and managed thereafter (Warner 134).

It entails testing of all neuropsychological impairments together with microscopic examination of biopsy brain tissues. The final definitive stage of diagnosis is the examination of all cognitive aspects of a suspected victim. These include problem solving abilities, functional ability, orientation, construction ability, attention, perpetual skills and overall strength of a patient’s memory (Green 245).

The most reliable technique used in examination is referred to as the mental state examination (MSE). This has been optimized in order to ensure that results are reliable. It gives a combination of both normal and neurological examinations.
Defensive mechanisms against this disease are yet to be put in place. Work towards the establishment of a specific particular measure is still under way.

Studies in the current medical practices have indeed offered some promising results in establishment prevention of Alzheimer disease (Harris 146). This entails balancing of factors that are linked with the occurrence of the disease. They include intellectual exercises, diet and proper individual care in the use of pharmaceutical products. If balance is maintained in the above areas, it becomes possible to curb the likelihood of the occurrence of Alzheimer.

Behavioral and vascular related factors such as smoking and hypertension also have a large part to play in this disease (Warner 102). It is possible to stop the risk factors by being careful of one’s health. In addition, uptake of cholesterol should be controlled. It is important for individuals to take healthy diets regardless of what they are used to. Alcohol should also be minimized although there is no particular limit which can be regarded to be completely safe.

At this point, it is worth to mention that people who are very active in terms of social interactions and playing brain games have a reduced risk of Alzheimer (Brill 243). This is explained by the theory of cognitive reservation. It is definite that mental activities tend to ‘play around’ with an individual’s brain in order to keep it sober enough in readiness to face challenges in life.

Pharmaceutical treatment is done to control the disease. There are several medications which are used to treat manifestations of Alzheimer’s disease. They are either based on correcting the fault of acetylcholine or receptors of boosting the mental activities of a patient (Warner 225). When the disease is full blown, there is no particular drug which can manage it. Reducing the effect of failing acetylcholine is the main significant activity known to affect this disease significantly (Lau and Berg 197).

Death of neurons is detected early enough to ensure that corrective measures are put in place before irreparable damage occurs in the brain. When a sufferer reaches high level of cognition impairments, medication is directed towards delaying the possible onset of the disease. Psychosocial interventions are also done. These are administered together with the above mentioned pharmaceutical treatments.

They include stimulation approaches, cognition boosters, emotional activators and behavioral modification (Brill 253). They are focused on rehabilitating the patient back to their normal lifestyle. Behavioral interventions reduce occurrences of abnormal behavior. This approach becomes successful when it is incorporated with aids of causing overall improvement of one’s condition. Most psychosocial therapies are based on the data obtained about a give customer.

On the other hand, emotional treatment is based on validation of lost sensory system. It is used to rehabilitate a person’s lost ability to define presence according to normal conditions. The treatment is aimed at helping such patients to call past events by comparing them with current ones. The validation therapy gives a patient an experience of what is true based on his or her senses. All these therapies are believed to be helpful although there is no enough proof of their working mechanisms.

The main aim of managing the disease is to bring back one’s ability to realize what is happening at a given period of time (Green 213). It includes providing information on the time and other realities which surround the capacities of a patient suffering from Alzheimer. Efficacy of improving cognition has recorded desirable results which are useful to both caregivers and the patient.

Giving care is essential to patients suffering from this health complication. It is evident that Alzheimer has no specific cure or treatment. This condition makes people unable to take care of themselves. It incapacitates individuals as time goes by. There are instances when a person becomes totally unable to do anything for themselves.

Given the effects of the disease, care giving is not optional here. Family members must ensure that the sufferer gets consistent care throughout their life time. This is done in all stages of the disease. The major goal of care giving is ensuring the safety of the patient. This is done through modification of the environment in which the person lives (Wagner 211). It reduces the burden of taking care of the person who has this particular disease.

Environmental modification entails the use of safety padlocks, placing important objects strategically and simplifying routine activities of the victim. In some cases, people are unable to feed themselves. Ethical issues crop up in the whole exercise of caring for a victim of Alzheimer.

These persons are highly vulnerable to being implicated by caregivers who may have ill motives. It is therefore important to come up with a good criterion for selecting a reliable care giver for your victim. Research reveals that individuals should be taught to take care of their own relatives because they have close links with them.

It is not easy to identify or rather diagnose the disease when it is at its early stages of development. The most reliable time to tell whether the disease has reached a critical stage is when cognitive impairments are noticed (Green 167).

At first, a person lives a normal life and it cannot be easy to explain the medical condition that a patient has gone through. In addition, symptoms progress towards a period of memory loss is indeed a mark of fatal Alzheimer. At the stage when it is impossible to live independently, everyone is convinced that the patient who suffers from Alzheimer needs total attention.

Life expectancy of persons living with the disease is always below 15 years of age (Brill 234). The disease is characterized by very low chances of survival for any person regardless of the choices they make in life. Medication is done to make sure that patients remain stable.

In other words, chances of survival beyond fifteen years are very minimal. Men will often have a shorter lifespan when diagnosed with the malady compared to women (Lau and Berg 254). The disease usually has a death risk of 70% among all the affected patients.
There are several future prospects in relation to this disease.

The efficacy of medical treatment of Alzheimer is yet to be made stable. More clinical trials need to be done in accordance with the developmental stages of the sickness. One of the most promising paths to take is that of pursuing immunotherapy. Clinical research ought to be focused towards the area of halting the pathogenesis of the disease. Besides, step by step inventions have to be followed in order to ensure that Alzheimer does not continue to incapacitate the population.

Works Cited

Brill, Marlene. Alzheimer’s Disease. New York: Benchmark Books, 2005. Print.

Green, Robert . Diagnosis and Management of Alzheimer’s Disease and Other Dementias. New York: Professional Comunications, 2005. Print.

Harris, Phyllis. The Person with Alzheimer’s Disease: Pathways to Understanding the Experience. Baltimore: The Johns Hopkins University Press, 2002. Print.

Lau, Lit-Fui and Stefan, Berg. Alzheimer’s Disease. Berlin: Springer, 2009. Print.

Warner, Morton. Alzheimer’s Disease: Policy and Practice Across Europe. Abingdon: Radcliffe Medical Press, 2002. Print.

Alzheimer’s disease (AD) is a common brain disease that attacks elderly people, especially those above 60 years. AD advances the victims gradually and the process is irreversible. The disease slowly destroys the parts of the brain that are responsible for cognition and thinking.

The disease may result in a serious situation in which the patient cannot even undertake the simple chores that he or she used to carry out (Green, 2005). Mrs. C in the case study is gradually developing AD and as a result, she requires medical intervention to prevent her condition from getting worse.

Mrs. C’s condition is likely to deteriorate as the disease advances to higher stages (Green, 2005). This is likely to have various effects on her close relatives, who include her husband, and their two daughters. Her husband is likely to bear the greatest burden if Mrs. C’s condition gets worse. Mrs. C carries out all the duties in their home; however, this is likely to stop because in the next few years, she might be unable to carry out her usual household chores such as preparing meals.

She will not be able to move around on her own and her cognition is also expected to deteriorate. Her husband will have to take over the duties Mrs. C used to perform in their house. Mrs. C’s husband will have to move her around, and prepare special meals for her. He will also have to understand the changes that come with AD; he will have to learn how to take care of her even after these changes have taken place.

The daughters, like her husband, will be forced to design their daily schedules to ensure that they create time to see her on a regular basis. Mrs. C’s husband is old and is not in a position to take care of the house and the sick wife at the same time.

This is why his daughters have to help him take care of their mother. After a few years, Mrs. C will not be able to wash her clothes or prepare food for her husband and herself. Their daughters will be responsible for these basic duties. They will also have to spend a lot of time with the patient to reduce the rate at which her condition is expected to advance.

Mrs. C’s condition is not likely to affect the relationship between her and her relatives if they are sensible toward her. The relatives may choose to keep the patient at home or take her to a nursing home.

If they decide to keep her at home, then they will need to set up a number of security measures such as: using secure locks on all the windows and doors, installing carbon monoxide detectors, use of smoke alarms, and ensuring no drugs, weapons, plastic bags or equipment are within her reach (Green, 2005). However, the best safety measure in the case of Mrs. C is to take her to a nursing home for the elderly. If her husband refuses, he should be convinced that it is best option for his safety.

If Mrs. C was my grandmother, then her sickness would affect my family as well. It would force my family to set a lot of time aside to attend to her. We would ensure that she does not become extremely affected by her condition. I would make sure that she gets the basic services that she requires, which may include: special food that is prescribed by a physician and improved personal hygiene. I would also ensure that we install safety measures for the sake of her security and that of other family members.

Reference

Green, R. C. (2005). Diagnosis and management of Alzheimer’s disease and other dementias. New York, NY: Professional Communications.

Alzheimer’s disease is a progressive disease in which memory impairment and disturbances in reasoning and perception are the primary symptoms. It is believed to be caused by an increase in a specific protein that causes nerve cell degeneration. The risk of having this disease increases after the age of 70. Increases age is the main risk factor for this disease. There are also genetic causes for this disease. High blood pressure, coronary artery disease, diabetes, etc are also other risk factors for Alzheimer’s disease (Bauer, p. 57).

Alzheimer’s disease is characterized by cognitive decline and a decrease in daily living activities. It is the most common type of dementia. Medications can help alleviate the symptoms of the disease but cannot reverse or slow the progression of the disease. Short-term memory loss and visual-spatial confusion are usually the first signs of this disease. Patients in the early stage of the disease become less energetic. There are other behavioral changes also like outbursts of violence (Brawley, p. 65).

The initial symptoms of the disease progress to more serious short-term memory loss and difficulty in moving around familiar areas. During the middle stage of the disease patients might retain some form of independence but require assistance in more complicated activities. Also, well-known skills and recognition of objects and person is diminished in this stage of the disease. The advanced stages of the disease are characterized by incontinence, bed fastness, and the inability to feed oneself. Patients require constant supervision and are not able to perform even the simplest tasks (Cox, p. 59).

Alzheimer’s disease affects the person with the illness and the caregivers. It is estimated that 1-4 people are caregivers. The disease has a long duration which impacts more on the caregivers. It can cause a great deal of emotional stress to caregivers. It also has a financial impact on those who provide care for patients suffering from Alzheimer’s disease. It is estimated that the national cost of caring for patients with Alzheimer’s disease is $100 billion (Hogg, p. 193). It can also indirectly cause lost productivity, absenteeism, and worker replacement.

Many people with Alzheimer’s disease do well at home during the initial stages. However, eventually, there is a need for long-term care facilities. Long-term care is defined as help from family and friends. It can also mean regular visits by home health aides. It might also mean moving the patient to an assisted or nursing home that can provide twenty-four medical attention (Janicki, p. 16).

There are two major types of long-term facilities for Alzheimer’s disease patients. One of them is a Nursing home that provides room and board with twenty-four-hour skilled care. A licensed nurse provides this type of care. There are special units for people with Alzheimer’s disease. The environments, activities, philosophy of care, and staff training are based upon the needs of Alzheimer’s disease patients.

Nursing homes usually have trained and supportive staff who know how to adjust to the patient. They have information about each patient to individualize care and eliminate behavioral symptoms. There are special activities that reduce anxiety and agitation. A nursing home has pleasing sights, sounds, and smells. They also have a low noise level and nonglare lighting. Some facilities also have security measures to prevent wandering (Dalton, p. 145).

Another type of long-term facility is assisted living. This type of facility is suitable for people who require personal care and general guidance but do not require any specialized medical care. They are good for people with moderate functional impairment. This type of long-term care promotes self-direction and participation in decisions. It also focuses on independence, privacy, and dignity. It attempts to create a home-based environment. It is an attractive option for patients who seek assistance and independence at the same time (Koenig, p. 174).

There are many types of assisted living facilities. Assistance in these facilities is characterized by helping the patient in bathing, grooming, transferring, toileting, laundry, cleaning, and meal reminders. Assisted living facilities for Alzheimer’s disease patients are known as “Special Care Units” (Marler, p. 14). The environment of such facilities is designed to make the patient safe and comfortable. Activities are meant to ensure that the patient will benefit. Some facilities accept people until they require special care. Others only accept people who are suffering from the initial stages of the disease.

There is a structured routine in these facilities. The staff has a particular time to gather lifestyle information about the patient. Safety measures are implemented to ensure a comfortable and safe surroundings. Activities help people in performing tasks such as making their bed and baking cookies. These activities provide satisfaction and productivity. Outdoor activities are also offered at such facilities. Staff members are trained to handle behavioral problems in this disease. Assisted living facilities are beneficial for patients who do not require specialized medical care and are at the early stages of the disease (May, p. 96).

Assisted living facilities offer many services. They can include providing one to three meals a day and monitoring medication. They also provide personal care and housekeeping. They have twenty-four-hour emergency care. They have medical, social, and recreational facilities. Looking for the best-assisted living facility is essential for caregivers. They should find out if the facility is licensed. They should also ensure what type of insurance facility is present in the facility. Their ability to respond to emergencies must also be analyzed by the caregivers (Robinson, p. 95).

Staff training is essential in choosing the type of assisted care facility. Caregivers should look at the staff turnover and their customer service skills. They also check if the staff members are adequately trained in assisting patients with memory and judgment problems. The atmosphere of the assisted living facility is also important since it should be observed how the residents socialize with each other. The opinions of other visitors and residents should also be listened to about the assisted living facility.

Finally, the appearance and environment of the building are important. The décor should be attractive. The floor plan must be easy to follow. There must also be facilities for accommodating wheelchairs and walkers. The availability of elevators and handrails is also important in deciding the best type of assisted living facility. The residence must be clean and free from odors. There should be appropriate heating and cooling. The security measures enforced at the assisted living facility must also be observed and monitored (Baxter, p. 20).

Alzheimer’s disease causes a decline in thinking, judgment, and problem-solving. It can also cause confusion and disorientation. It causes difficulty in maintaining normal behaviors. It can cause inappropriate social situations. The patient can become a danger to himself. Anxiety, paranoia, and hallucinations are psychotic behaviors displayed in patients. Behavior problems require a modification of lifestyle and environment. Wandering, hiding things, anger, belligerence, hallucinations, and eating problems are some of the behavioral problems that have to be handled (Bass, p. 20).

Alzheimer’s disease is a progressive disorder that has no cure. It affects caregivers and causes direct and indirect losses. Caregivers must eventually decide on long-term care. Long-term care usually consists of nursing homes and assisted living facilities. Assisted living facilities are beneficial for patients in the early stages of the disease. They are the best option for patients who do not require a specialized medical skills. There are many types of assisted living facilities. Assistance in these facilities is characterized by helping the patient in bathing, grooming, transferring, toileting, laundry, cleaning, and meal reminders. Assisted living facilities for Alzheimer’s disease patients are known as “Special Care Units”. The environment of such facilities is designed to make the patient safe and comfortable. Activities are meant to ensure that the patient will benefit.

Choosing the best type of long-term care can be difficult for caregivers. Assisted living facilities are the best option for people with early stages of the disease. Nursing home facilities are best for patients who suffer from advanced stages of the disease. Alzheimer’s disease can cause emotional and financial stress to the patient and the caregivers. However, there are many choices available that can improve the quality of life.

Works Cited

1. Bass, D. (2002). Content and Implementation of a Caregiver Assessment. [Issue Brief]. Washington, D.C.: Administration on Aging.
2. Baxter, E. (2000). Caregiver assessment: Learn about the caregiver, distinct from the person with dementia. Alzheimer’s Care Quarterly, 1 (3)
3. Bauer, A.M, Alzheimer’s disease and Down Syndrome: A Review and Implications for Adult Services Education and Training of the Mentally Retarded, 1986
4. Brawley, E.C. Designing for Alzheimer’s Disease – Strategies for Creating Better Care Environments. New York: Wiley (1997)
5. Cox, S. Home Solutions: Housing & Support for People with Dementia London: The Housing Associations Charitable Trust (1998)
6. Dalton, A.J. Prevalence of Dementia and Impact on Intellectual Disability Services Mental Retardation, 2000
7. Hogg, J. Practice Guidelines for the Clinical Assessment and Care Management of Alzheimer’s disease and Other Dementias among Adults with Intellectual Disability Journal of Intellectual Disability Research, 1996
8. Janicki, M.P. Care Management, Diagnostic and Epidemiologic Considerations in Adults with Intellectual Disabilities and Alzheimer Disease British Journal of Developmental Disabilities, 1996
9. Koenig, B.R. Aged and Dementia Care Issues for People with an Intellectual Disability: Best Practices (vol. 2). Brighton, South Australia: MINDA, Inc. (1995)
10. Marler, R., Down’s Syndrome and Alzheimer’s Disease: A Guide for Carers. London: Down’s Syndrome Association (1994).
11. May, H.L., Alzheimer’s disease and Down Syndrome: A Manual of Care Wrentham, Mass.: Alzheimer’s Committee of Wrentham Developmental Center (1996)
12. Robinson, A., Understanding Difficult Behaviors: Some Suggestions for Coping with Alzheimer’s Disease and Related Illnesses. Geriatric Education Center of Michigan (1999 rev.)

There are many superficial similarities between Alzheimer’s disease and Parkinson’s disease primarily in some symptoms and age-group of persons afflicted by these two diseases. Nonetheless, these two are inherently distinct and distinguishable from each other in many aspects such as etiology and treatment, for example.

Alzheimer’s disease is a progressive and lethal neurodegenerative disorder characterized by cognitive and memory decline (Cummings, 2004). Due to this performance of daily activities are severely affected. In addition, a range of neuropsychiatric and behavioral symptoms are also observed. The prevalence of the disease is notable since in the United States alone there are approximately 4.5 million sufferers in 2000 (Hebert et al., 2003).

Parkinson’s disease is likewise a neurodegenerative disorder manifested by motor function symptoms such as tremor and rigidity accompanied by dementia in advanced cases although there are nine differential diagnoses of Parkinsonism (Rao et al., 2006). The prevalence of Parkinson’s disease in the US population is pegged at 0.3 percent (de Lau, 2004) and one million in United States alone (Zigmond & Burke, 2002).

This paper aims to identify the characteristics of Alzheimer’s and Parkinson’s diseases including their etiology, pathology and pathophysiology, clinical presentations, natural history and prognosis, diagnosis, treatment and other current and relevant information with the purpose of establishing the similarities and differences between the two diseases.

Regarding etiology, Alzheimer’s and Parkinson’s diseases share common characteristics since both are induced at some level by genetic conditions. Alzheimer’s disease has a complex hereditary relationship. In 20 percent of early-onset cases of Alzheimer’s disease, it is found to be inherited in autosomal manner although in late-onset cases genetic factors are said to play a role in the incidence of familial aggregation. There are three genes identified to be responsible in early-onset Alzheimer’s disease; these are APP, presenilin 1 and presenelin 2 which are inherited in autosomal dominant manner (Brice, 2004). APP is located in chromosome 21 while presenelin 1 is involved in point mutations while presenelin 2 are not associated with such genetic aberrations. In late-onset cases of Alzheimer’s disease the gene ApoE is implicated as a risk factor (Brice, 2004).

Parkinson’s disease, on the other hand, is also considered to be brought about by the interaction between various genes and environmental factors which are currently not yet fully researched. Nonetheless, there are several loci being studied for their association with familial parkinsonism which are PARK1-PARK11. Four of seven genes from these loci were found to cause autosomal dominant -synuclein. The other three, parkinsonism; these are LRRK2, UCHL1, NURR1, and namely DJ1, PINK1 and parkin, were identified as inducing autosomal recessive disorder (Tolosa et al., 2006).

In terms of pathology and pathophysiology, Alzheimer’s and Parkinson’s disease largely differ. Alzheimer’s disorder experts point to the generation and increase of beta-amyloid peptide as the pathological characteristics of the disease according to Cummings (2004). This is supported by the observation of amyloid precursor protein mutations in cases of late-onset Alzheimer’s disease and the increase in the production of beta-amyloid peptide are invariably traced back in all mutations associated with Alzheimer’s disease (Hardy & Selkoe, 2002).

On the other hand, Parkinson’s disease is characterized by loss of DA or dopamine neurons which are located in the substantia nigra pars compacta (SNpc) according to Zigmond & Burke (2002). The authors added that up to 60 percent of DA neurons are lost even in mild Parkinson’s disease patients while remaining neurons may become dysfunctional which result to the 80 percent total loss of DA neurons in the corpus striatum. Another pathological sign of this disease is the Lewy body which is an eosinophilic inclusion located inside neurons which are associated with brain regions showing severe neuron loss (Zigmond & Burke, 2002).

For clinical presentations, a range of symptoms are involved in both Alzheimer’s and Parkinson’s. While the primary clinical presentations of Alzheimer’s are cognitive or mental dysfunction, Parkinson’s is characterized more of motor function abnormalities. Alzheimer’s disease is commonly associated with recent memory loss, aphasia and apraxia. Advance cases manifest psychiatric or behavioral abnormalities, extrapyramidal syndrome, epileptic attacks and myoclonia (Brice, 2004). Cummings (2004) put the classical features of Alzheimer’s memory impairment of amnesic kind, language decline and visuospatial problems with accompanying motor and sensory disorders such as walking problems and seizures.

On the other hand, Parkinson’s disease is characterized by shaking or trembling, stiffness and slowness of movements. In addition to these motor function aberrations are mental or cognitive features such as dementia or dysautonomia. Forty percent of Parkinson’s disease patients may suffer depression. Furthermore, around half of patients experience pain and sensory symptoms secondary to the degree of motor impairment mentioned above. However, nine differential diagnoses is present in Parkinson’s disease with different sets of signs and symptoms. For example, idiopathic Parkinson’s disease presents with tremor, bradykinesia, rigidity, poor gait and micrographia while vascular parkinsonism can be characterized by fixed discrepancies from previous events, and dementia with Lewy bodies diagnosis can be manifested by impaired attention and syncope among other persistent symptoms (Rao et al., 2006).

In terms of natural history and prognosis, Parkinson’s disease provides a wider range of characteristics compared to Alzheimer’s which is due to the various differential diagnoses that are available to the latter. For instance, idiopathic Parkinson’s disease includes historical features such as difficulty with activities, stiffness and tremor. Drug-induced parkinsonism involves previous use of a causative chemical while normal-pressure hydrocephalus requires ataxia, urinary incontinence and dementia. On the other hand, Alzheimer’s disease has limited natural history characteristics that are indicative of the disease. Nonetheless, problems in global cognitive ability and episodic memory are somewhat implied according to Backman et al. (2005).

Regarding diagnosis, Parkinson’s understandably involves various symptoms and characteristics for the establishment of diagnoses included in the disease spectrum while Alzheimer’s does not necessitate as much such that different tests are required for the former compared to the latter. In Parkinson’s disease a series of tests are needed to determine if the presented case is idiopathic Parkinson’s disease, drug-induced parkinsonism, vascular parkinsonism or any of the other six diagnoses. In order to establish such diagnoses, genetic testing may be used to evaluate the seven genes located in the PARK loci described above. Drug challenge more specifically dopaminergenic responsiveness, neurophysiology detailing relevant brain motor functions, autonomic function testing such as cardiovascular, olfactory test for hyposmia, computed tomography and magnetic resonance imaging are all very useful tools for the diagnosis of Parkinson’s disease (Tolosa, 2006).

On the other hand, the classic features or symptoms described above are initially used for Alzheimer’s disease diagnosis. Next to this is the assessment of psychological or behavioral disturbances that the patient may present such as performance of daily activities, mood swing, apathy, psychosis and agitation. Laboratory tests for the determination of dementia include thyroid-function tests, serum electrolyte, blood glucose, serum vitamin B12 measurement, blood count, blood urea nitrogen measurement and liver-function tests (Cummings, 2004). In addition to these, other specialized laboratory tests for syphilis, erythrocyte and human immunodeficiency virus are also necessary to establish dementia. Computed tomography and magnetic resonance imaging can be used to diagnose Alzheimer’s disease while positron-emission tomography and single-photon-emission computed tomography are used for differential diagnosis dementia-related diseases.

In terms of treatment, understandably Parkinson’s disease and Alzheimer’s disease require their own set of chemical and other forms of intervention. Both treatment regimens include circumventing the biochemical processes involved in the induction of the disease while others relieve or suppress some of the pain or symptoms. For Alzheimer’s disease the use of antioxidants such as vitamin E or alpha-tocopherol (Sano et al., 1997); an N-methyl-D-aspartate antagonist called memantine(Danysz & Parsons, 2003); cholinesterase inhibitors such as tacrine, rivastigmine, donepezil and galantamine are being both recommended and evaluated at the present (Watkins et al., 1994).

On the other hand, medications for Parkinson’s disease that are FDA-approved include anticholinergics such as benztropine and trihexyphenidyl, carbidopa or levodopa, COMT inhibitors such as entacapone and tolcapone, dopamine agonists such as bromocriptine and pergolide, MAO-B inhibitors such as selegiline and rasagaline, and NMDA receptor inhibitor such as amantadine (Rao et al., 2006)

Current issues that are facing the diagnosis and treatment of Parkinson’s disease include the low level of diagnosis certainty necessitating newer technology, exploring nonpharmacologic treatment strategies and cost-effectiveness of recommended procedures (Delagarza, 2003). According to Tolosa (2006), the clinical diagnostic uncertainty for Alzheimer’s disease is high at the early stage of presentation. This fact results to reclassification of 30 percent of patients initially diagnosed with the disease (Tolosa, 2006). According to Rao et al. (2006), nonpharmacologic interventions may not be the magic bullet for Parkinson’s but can be helpful in sustaining the patient’s welfare. Cost-effectiveness of modern diagnostic methods based on computed tomography and magnetic resonance imaging are not yet established (Tolosa, 2006).

On the other hand, the elucidation of preclinical characteristics of Alzheimer’s disease, concerns on fatal cases with emphasis on health maintenance and treatment of related complications, and the importance of the role of caregivers for the welfare of affected persons (Cummings, 2004). Cummings adds that septicemia, pneumonia and other diseases may lead to death in Alzheimer’s cases necessitating development of better health maintenance. According to Backman et al. (2005), there is a need to combine predictors of Alzheimer’s disease from multiple behavior and biological aspects for the improvement of diagnosis involving preclinical characteristics.

In conclusion, upon identification of the different characteristics of Alzheimer’s and Parkinson’s disease regarding etiology, pathology and pathophysiology, clinical presentations, natural history and prognosis, diagnosis, treatment and other current issues, the unique features of each disorder were obtained. Although both are neurodegenerative diseases and afflict the same age group, the etiology, pathophysiology, diagnosis and treatment are inherently divergent including the current issues besetting the strategies for their management.

Reference List

1. Backman, L., Jones S., Berger, A.K., Lauka, E.J and B.J. Small. (2005). Cognitive impairment in preclinical Alzheimer’s Disease: A meta-analysis. Neuropsychology 14 (4), 520-531.
2. Cummings, J.L. (2004). Alzheimer’s disease. The New England Journal of Medicine 351, 56-67.
3. de Lau, L.M., Giesbergen, P.C., de Rijk, M.C., Hofman A., Koudstaal P.J., and M.M. Breteler. (2004). Incidence of parkinsonism and Parkinson disease in a general population: the Rotterdam Study. Neurology 63, 1240-4.
4. Danysz W., and Parsons C.G. (2003). The NMDA receptor antagonist memantine as a symptomatological and neuroprotective treatment for Alzheimer’s disease: preclinical evidence. Int J Geriatr Psychiatry 18, S23–S32.
5. Delagarza, V.D. (2003). Pharmacologic treatment of Alzheimer’s Disease: An update. American Academy of Family Physicians. Web.
6. Hardy J. and D. J. Selkoe. (2002). The amyloid hypothesis of Alzheimer’s disease: progress and problems on the road to therapeutics. Science 297,353-6.
7. Hebert L.E., Scherr P.A., Bienias J.L., Bennett D.A., and D.A. Evans. (2003). Alzheimer disease in the US population: prevalence estimates using the 2000 Census. Arch Neurol 60, 1119-22.
8. Mohs, R.C. and V. Haroutunian. (2002). Alzheimer’s disease: From earliest symptoms to end stage. In Neuropsychopharmacology: The Fifth Generation of Progress. Eds. K.L. Davis, D. Charney, J. T. Coyle and C. Nemeroff.American College of Neuropsychopharmacology.
9. Rao, S.S., Hofmann, L.A. and A. Shakil. (2006). Parkinson’s Disease: Diagnosis and treatment. American Academy of Family Physicians. Web.
10. Sano M., Ernesto C., Thomas R.G., et al. (1997). A controlled trial of selegiline, alpha-tocopherol, or both as treatment for Alzheimer’s disease. N. Engl. J. Med. 336,1216-22.
11. Tolosa, E., Wenning, G. and W. Poewe. (2006). The diagnosis of Parkinson’s disease. Lancet Neurol. 5, 75-86.
12. Watkins P.B., Zimmerman, H.J., Knapp, M.J., Gracon, S.I., and L.W. Lewis. (1994). Hepatotoxic effects of tacrine administration in patients with Alzheimer’s disease. JAMA 271, 992-8.
13. Zigmond, M.J. and R.E. Burke. (2002). Pathophysiology of Parkinson’s disease. In Neuropsychopharmacology: The Fifth Generation of Progress. Eds. K.L. Davis, D. Charney, J. T. Coyle and C. Nemeroff.American College of Neuropsychopharmacology.

A nurse doesn’t only provide nursing care. She also, in some cases, has to teach her patient and/or her patient’s relatives the basic nursing care needed to be perceived especially in the absence of a health care provider. It is a challenging experience for a nurse to give health teaching to an Alzheimer’s patient because these patients are totally disoriented and confused about the current setting, and have speech difficulties (Russell, et al, 2007).

This tells us that the possibility of a successful health education for an Alzheimer’s patient is a few percent lesser than a teaching plan for a patient without mental and psychological disturbances. That’s why it is important for us to assess first our patient, to know what, where and how to start conducting our teaching plan for them.

Assessment of Learner

The learner or the subject of this teaching plan is an Alzheimer’s patient with diabetes mellitus. He is 55-year-old man suffering from early stage or mild Alzheimer’s disease. His symptoms are: minor cognition and memory alteration as evidenced by confabulation (filling in memory gap), minor anterograde amnesia (forgets recent memory) and retrograde amnesia (forgets distant memory), and loss of orientation to some daily tasks like peeling an apple or changing a television channel. He also has communication problems, as evidenced by difficulty speaking and understanding complex instructions/materials (Russell, et al, 2007).

It is important to give health teaching to an Alzheimer’s patient with diabetes mellitus about diabetic glucose monitoring because Insulin metabolism is important for proper central nervous system functions because it acts on the neural impulse transfer, which affects the person’s sensory and motor abilities (Sabayan, et al, 2007), and through his independence in monitoring his blood glucose level, he will be able to help himself in getting reoriented with reality, practice performing his usual daily activities and watch his diet out to decrease elevation of blood glucose level.

Before conducting the teaching plan, the patient was assessed of his orientation to reality; when asked “Do you know where you are?” and “What time is it?” the patient responded correctly but it took him 2 minutes before he was able to answer my questions. His level of understanding was tested when he was asked, “If you are able to understand me, can you tell me why you need to monitor your blood glucose?” and answered that he needed the test to know if he’s gone beyond is allowable blood glucose level. His memory was tested when he was asked, “Can you tell me again where we are and what time it is?” and replied the same answer he gave me earlier. After these preliminary patient assessments, we were ready to proceed with the teaching plan.

Learner’s Prior Level of Knowledge

The patient is aware that he has an Alzheimer’s disease and diabetes mellitus. He knows that he had had previous blood glucose monitoring in the past that he does alone, but this ability had deteriorated ever since the presence of his disease. He knows the purposes and some of the steps and needs to be taught again to regain his independence in monitoring his blood glucose level.

Learner’s Perception of Learning Needs

The patient is suffering from early stage or mild Alzheimer’s disease, and given the symptoms mentioned in the previous pages, it is important to improve the areas where he is still capable to do independently. The patient knows that he needs to be taught again on how to monitor his blood glucose as he said that he would want to do it again if only he can remember the procedures.

Learner’s Attitude towards Learning

The patient was keen and observant during the entire duration of assessment and teaching plan. He is suggesting that he wants to regain his independence in monitoring his blood glucose, as he knows how important it is to maintain an allowable blood glucose level. The patient, although was very slow in responding in words and in actions, was seen with great interest, as he hasn’t shown any signs of irritability. He was anxious in the start upon knowing that he will be pricked, but his anxiety was alleviated when he knew that only a few drops of blood is needed to perform the actual monitoring.

Social, Cultural and Physical factors that may affect Learning

Some of the factors that will affect the patient’s learning are his minor cognition and memory alteration as evidenced by confabulation, minor anterograde amnesia and retrograde amnesia, and loss of orientation to some daily tasks. He also has communication problems, as evidenced by difficulty speaking and understanding complex instructions/materials (Russell, et al, 2007). The patient is a 55-year-old man that would require, plus his mental problems, the importance of giving slow instructions and using simple words. He is and American-speaking patient. His families regularly visit him and maintaining close family ties with strong faith in Catholicism. His hobby includes reading and watching movies, and is a former writer for a publication.

Nursing Diagnosis

Ineffective health maintenance related to cognitive impairment as evidenced by observed and reported inability to take responsibility for meeting basic health practices (Doenges, et al, 2004).

Learner Objectives

Short-term goal

After the teaching plan, the patient will describe the importance of and demonstrate the proper ways of monitoring his blood glucose level.

Intermediate goal

On the succeeding time when the patient is scheduled to monitor his blood glucose level, he will perform the procedure the right way with minimum supervision.

Long-term goal

On the succeeding times when the patient is scheduled to monitor his blood glucose level, he will perform the procedure the right way without any supervision at all.

Topic and Outline

1. The patient will be taught of the equipments and their uses. The equipments that were used were a carrying case (containing all the necessary equipments), lancing device (depresses the lancet onto the skin), lancet (pricks the skin), test strip (holds the blood before testing by meter), self-test logbook (for baseline data) and the glucometer (measures the blood glucose level). Other equipments include dry cotton, surgical tape and pen.
2. The patient will be taught of the preliminary preparations before proceeding with the procedure. The first thing to do before the actual monitoring is to prepare all the materials because he will need all the equipments near him at all times. The next thing is to tell the patient to clean the lancing device with an antiseptic solution. After he has prepared these things, the next thing to do is to ask him to wash his hands to keep clean the procedure.
3. The procedure will first be discussed, and then demonstrated to the patient. After the patient has attached the lancet to the lancing device, he will then prick his fingertip in a very light manner. He will be asked to get the test strip and allow a drop of blood onto its surface. Then, he needs to cover and put pressure on the prick site with dry cotton and surgical tape. He then has to put the test strip on the glucometer and wait for a few seconds. When the glucometer displays an unchanging value, this is already his blood glucose level. Before meals, the normal range is between 90 to 130 mg/dL. After meals, the normal values are 180 mg/dL and below. After the procedure, he needs to be sure to note on his self-test logbook the result as this provides the baseline data of his blood glucose monitoring.

Methods and Materials

Resources used

The resources that were used were my knowledge and experience. We also used posted cardboard in his room with simplified step-by-step procedure of performing blood glucose level monitoring for his future reference, in case he gets lost along the middle of the procedure. A handout, especially prepared by myself, was given to the patient as a guide during the process of teaching plan.

Equipments used

The equipments that were used were a carrying case (containing all the necessary equipments), lancing device (depresses the lancet onto the skin), lancet (pricks the skin), test strip (holds the blood before testing by meter), self-test logbook (for baseline data) and the glucometer (measures the blood glucose level). Other equipments include dry cotton, surgical tape and pen.

Teaching strategies used

The teaching strategies that were used were discussion (before demonstration) and demonstration (actual return demonstration of the patient). The patient was given a cardboard of step-by-step procedure that he may need in the future.

Teaching sessions

The teaching session for the first encounter is approximately 20 minutes, covering all the activities from introducing myself to leaving the patient learned about the teaching plan. The succeeding meetings will depend on how quick the patient understands the teaching plan for the first time, and on how much memory he stores based on the discussion and demonstration.

Evaluation of Teaching Plan

From the first strategy of teaching that was used, which was discussion, the patient’s cognition was improved. His memory and understanding were given importance. From the demonstration strategy of teaching, the patient’s psychomotor was improved. His skills and ability to incorporate the discussion to the demonstration was given importance at this instance. Following the teaching plan, I made sure that I gave him the cardboard that contained a simplified step-by-step instructions that he might use for future references. The handout that we used during the duration of the teaching plan can be used by his accompanying relatives so they could guide the patient in the future in the absence of a health care provider.

Interpersonal Process Recording

References

Doenges, M., Moorhouse, M., Murr, A. (2004). “Nurses Pocket Guide: Diagnoses, Interventions and Rationales, 9^th Edition”. Philadelphia.

Hurd, R. (2007). Blood glucose monitoring. Retrieved October 7, 2008, from Healthline Networks. Web.

Russell, D., Segal, J., White, M., (2007). Alzheimer’s Disease: Signs, Symptoms and Stages. Web.

Sabayan, B., Foroughinia, F., Mowla, A., Borhanihaghighi, A. (2008). Role of Insulin Metabolism Disturbances in the Development of Alzheimer Disease: Mini Review. American Journal of Alzheimer’s Disease and Other Dementias, Vol. 23, No. 2.

Introduction

Alzheimer’s disease is a late-age congenital (since or even before birth) progressive neurodegenerative disorder, particularly affecting the brain at regions associated with higher mental functions such as neocortex and hippocampus region in forebrain. Pathologically, it manifests as extra-cellular deposits of β-amyloid proteins, derived by the action of enzymatic proteins, Precenilins, on amyloid precursor proteins (APP’s) produced in neurons.

These changes accompany an impairment of cognitive functions (memory, sense). Most of the investigations on amyloid plaques, a kind of neural coating, reveal presence of high amounts of unique Aβ proteins, whose amounts go up in diseased brain neurons. Two sub-types of this protein were immunologically detected and termed as Aβ₄₂ and Aβ₄₀. These changes bring about a cascade of events leading to inflammation and neuro-toxicity, which progress as release of harmful cytokines, neuritic membrane injury, ionic homeostasis, and oxidative injury.

Consequently, imbalance in protein kinase/phosphorylase signal transduction results in hyperphosphorylation and deformation of neurofibrilary micro tubular protein, known as tau, which leads to neurotransmitter deficits and dementia, a typical abnormal state of brain. The production and/or deposition of Aβ proteins in cerebral fluid and is linked with genetic mutations of at least four genes located in human chromosome #1, 14, 19 and 21 (Selkoe, 2001).

Review of literature

Six peer reviewed research articles related to genomic/proteomic analyses, and diagnostic aspects of Alzheimer’s are discussed. A complete genome analysis of Alzheimer’s disease was carried out by Kehoe et al. (1999). Usually, if proper markers for disease-related mutated genes are available, pre-natal prognosis of the disease through genetic counseling can be done. Such gene-associated markers have been characterized, in particular the apolipoprotein E gene, which was linked to chromosome# 19, and was responsible for accumulation of Aβ by way of binding to this protein. In this study, genome scan was carried out in 600 diseased sibling pairs.

Semi-automated fluorescent genomic mapping of each autosome and X chromosome, in which labeled marker DNA’s, corresponding to specialized chromosomal locations, called micro-satellites (specific repeats of consensus evolutionary DNA sequences), were used to detect presence of apolipoprotein E gene-linked marker. For this, lymphoblastoid cells (from leukocytes) were grown in cell culture medium, DNA was extracted and genomic analysis was done using a database.

It was revealed that apart from chromosome #19, apolipoprotein gene sub-types were also present in chromosome #1, 9 and 10. This suggests a high degree of linkage within the chromosome regions carrying apolipoprotein E gene. This finding can help in detection of the most causative gene or marker in chromosomes (#1, 9 and 10), other than what has been considered earlier (#19) for the detection process.

Another important and new discovery in this area has been to characterize the Alzheimer’s disease-specific protein biomarkers as diagnostic tools for early detection. According to Finehout, Franck, Choe, Relkin, & Lee (2007) a comparative proteomic analysis of cerebrospinal fluid, collected from diseased and healthy persons, gave clue on differential protein expression in the diseased tissue. Proteins from 34 patients and 34 normal control subjects were subjected to 2-dimentional electrophoresis, in which first dimension of protein separation is based on isoelectric points of the proteins, and then proteins are further resolved in second dimension by charge and molecular weights.

The proteins that were exclusively detected in the diseased samples were further identified by mass spectroscopic methods and by matching with protein database. Twenty three clear spots were found expressed in Alzheimer tissues. The prominent proteins identified were, Aβ transported proteins (including albumin), inflammation-related proteins, proteolytic enzyme inhibitors like anti-trypsin, and some neuronal membrane proteins. These are probably the largest ante mortem pathological biomarkers to be used for clinically relevant diagnostic assays.

Apart from genomic and proteomic diagnosis, anatomical methods like magnetic resonance imaging (MRI) of regions affected at very early stage can be used for early in vivo detection. Dickerson et al. (2001) carried out MRI to detect extent of hippocampal and entorhinal atrophy (wasting away of the tissue) in 34 healthy controls, 28 patients with cognitive complains not amounting to clinical dementia, and 16 patients with mild Alzheimer.

Mean normalized hippocampal and antorhinal volumes from both hemispheres were computed and statistically treated. The volumetric values significantly increased in both the affected groups compared to the controls, though the difference was not so significant between the two affected groups. Hence, the volumetric changes start much early even before mild cognitive impairment, such as age-associated memory loss. Such neuro-volumetric analysis would be useful anatomical biomarker for early diagnosis.

As mentioned, apolipoprotein proteins are related to Aβ proteins deposition, whose serum level can be monitored as biochemical biomarker for early diagnosis. Merched, Xia, Visvikis, Serot & Siest (2000) carried out an investigation on relative concentration of this protein in serum. For this, blood from 98 patients and 59 healthy elderly people were analyzed for cholesterol, triglycerides, and serum apolipoprotein A and B, the later by immunological methods.

The serum apolipoprotein A, but not B, was quite low in serum collected from diseased compared to healthy controls. Another interesting feature was that in patients, with mutated apolipoprotein E genes and who are more prone to the disease, the serum level of apolipoprotein A correlated with severity of Alzheimer’s disease. As this protein level goes up in cerebrospinal fluid in the patients, it was proposed that enhanced passage from blood to brain fluid may account for decrease level in serum.

In another study, serum homocysteine level, generally known to be associated with cardiovascular diseases, has been shown to correlate with general dementia and Alzheimer’s disease (Seshadri et al., 2002). Plasma total homocysteine level was measured in 1092 subjects without dementia. Within eight years, those individuals having >14 µmol L^-1 baseline value, exhibited clinical symptoms of the disease and dementia.

Lower serum of folate a vitamin precursor and vitamin B₆ and B₁₂ are associated with elevated homocysteine level, but their levels could not be associated with the progression of the disease. Interestingly, this attribute was independent of the risk prone genotype and every population had the homocysteine-related development of dementia. Hence, plasma total homocysteine appears to be another crucial biochemical marker for both cardiovascular and Alzheimer’s diseases.

Several independent lines of study suggest that toxicity and neuro-degeneration action of Aβ proteins is mediated through production of reactive oxygen species (ROS). Hence, enzymes that quench ROS also protect neurotoxicity. One such enzyme discovered is NAD(P)H:quinone oxidoreductase (QR). In a study post-mortem tissue were obtained from 6 patients and 5 healthy persons (Wang, Santa-Cruz, DeCarli & Johnson. 2000).

After tissue homogenization, the QR level was determined by immunohistochemical straining and by Western blot analysis, using specific anti-serum raised against QR. The hippocampal neurons stained heavily in the patients’ samples, but not in controls. In accordance to this result, the patients’ brain samples also positively reacted with anti-QR-antibody, while much lower cross-reactivity was found in healthy controls. Hence, QR level can become another important enzyme-marker and can be adopted to use ante mortem for an early diagnosis of Alzheimer’s disease.

Conclusion

The biochemical and genetic basis of Alzheimer’s disease and associated dementia were discussed, and six articles related to genomic, proteomic, anatomical and biochemical markers for early detection were reviewed. The genetic marking of the prone-population is possible by epidemiological and anthropological investigations. Proteomic markers can further verify the onset and progression of disease in the prone population. Biochemical biomarkers and anatomical imaging can help confirm the disease symptoms, not only in prone but also in those populations in which other abnormalities are associated with dementia. Finally, new drugs can be designed and their efficacy can be monitored at preclinical and clinical trials.

References:

Dickerson, B.C., Goncharova, I., Sullivan, M.P., Forchetti, C., Wilson, R.S., Bennett, D.A., et al. (2001). MRI-derived entorhinal and hippocampal atrophy in incipient and very mild Alzheimer’s disease. Neurobiology of Aging, 22, 747–754.

Finehout, E.J., Franck, Z., Choe, L.H., Relkin, N., & Lee, K.H. (2007). Cerebrospinal fluid proteomic biomarkers for Alzheimer’s disease. Annals of Neurology, 61, 120–129.

Kehoe, P., Vrieze, F.W., Crook, R., Wu, W.S., Holmans, P., Fenton, I, et al. (1999). A full genome scan for late onset Alzheimer’s disease. Human Molecular Genetics, 8 (2), 237-245.

Merched, A., Xia, Y., Visvikis, S., Serot, J.M., & Siest, G. (2000). Decreased high -density lipoprotein cholesterol and serum apolipoprotein AI concentrations are highly correlated with the severity of Alzheimer’s disease. Neurobiology of Aging, 21, 27–30.

*Selkoe, D.J. (2001). Alzheimer’s disease: Genes, proteins, and therapy. Physiological Reviews, 81 (2), 741-766.

Seshadri, S., Beiser, A., Selhub, J., Jaques, P.F., Rosenberg, I.H., D’Agostino, R.B., et al. (2002). Plasma homocysteine as a risk factor for dementia and Alzheimer’s disease. The New England Journal of Medicine, 346 (7), 476-483.

Wang, Y., Santa–Cruz, K., DeCarli, C., & Johnson, J.A. (2000). NAD(P)H:quinone oxidoreductase activity is increased in hippocampal pyramidal neurons of patients with Alzheimer’s disease. Neurobiology of Aging, 21, 525–531.