This sample essay explores the neurological condition known as Alzheimer’s Disease, as well as an overview detailing the symptoms and possible treatment. The essay is an example of the nursing papers available from Ultius and using by students during their medical training.
Background and history of Alzheimer’s Disease
Alzheimer’s disease (AD) is a neurodegenerative condition that impacts patient’s emotional stability and physical well-being. It accounts for roughly two-thirds of all dementia cases. A chronic condition that worsens over time, Alzheimer’s advances in stages: starting with momentary memory loss; proceeding to episodes of disorientation, incoherence, and behavioral abnormalities; and culminating with social withdrawal and loss of bodily functions towards the end of a patient’s life. The speed at which the disease takes hold of an individual can vary, but post-diagnosis life expectancy generally ranges from 3.2 to 6.6 years (Todd).
The exact causes of Alzheimer’s are uncertain, though genes are believed to play a significant role in the risk factor. People with histories of depression, hypertension, and injuries to the head are also more prone to Alzheimer’s. When symptoms are first exhibited, they’re often misread for normal signs of aging. There is currently no cure for Alzheimer’s, nor are there any pharmaceutical drugs to prevent the onset or suppress the symptoms, but it’s believed that mental and physical exercise can reduce one’s risk of developing the disease.
As of 2015, as much as 70% of the world’s 47.5 million dementia sufferers have been affected with AD (“Dementia”). In the vast majority of cases, the onset of Alzheimer’s begins after age 65 and affects roughly 5 million people in that age group (“Alzheimer’s Disease”). The disease was named in 1906 after German psychiatrist Alois Alzheimer (1864–1915), who first diagnosed the symptoms several years beforehand in one of his patients, Auguste Deter: a dementia-stricken fiftysomething woman who’d been placed in a mental institution by her husband.
The character and stages of the disease
The disease impacts both the long and short-term memory. Some of the earliest symptoms of Alzheimer’s include minor moments of forgetfulness which are often just seen as common among people over a certain age. In fact, the diminished cognition that presages Alzheimer’s can manifest for nearly a decade before an individual’s condition meets the clinical classification of the disease. Aside from the small number of cases where distinguishing genetics have been found in Alzheimer’s patients, little has been determined about the root causes of the disease.
Once the disease has taken hold, the individual will typically exhibit problems with semantic memory—the ability to remember the meaning of things—and short-term memory. In the morning, for example, an AD-stricken widowed man could agree to an afternoon picnic with his daughter and grandchildren, only to be in the midst of eating lunch by himself when she arrives to pick him up. Note that he doesn’t have trouble remembering how to fix his own lunch because that falls under the category of implicit memory: the knowledge that people call upon through habit and repetition—such as tying shoelaces or taking a shower—rather than awareness.
The three stages of Alzheimer’s Disease
- Early stage – marked by sporadic periods of forgetfulness; a random inability to remember names of loved ones; and confusion toward non-routine situations.
- Middle stage – in which a person has trouble sleeping; difficulty retaining newly learned info; a tendency to get lost in public, either by foot or by wheel; and a more pronounced confusion toward things in general.
- Advanced stage – characterized by incoherent talk; fidgety, nervous, paranoid behavior; a tendency to repeat oneself in conversation; and a severely diminished ability to think clearly.
The early symptoms are usually only noticed by friends and loved ones. Gradually, however, the brief moments of forgetfulness give way to an uncharacteristic lack of detail, and by the middle stage, the symptoms become readily apparent to anyone familiar with AD.
Early vs. late-onset Alzheimer’s Disease
Early-onset Alzheimer’s—alternately known as Familial Alzheimer’s Disease (FAD)—is the less common form of the disease that accounts for only five percent of all cases. The onset occurs in people between the ages of 30 and 60, and while its cause is often unknown, it’s sometimes attributed to genetic mutations on the chromosomes 1, 14, and 21. A child with at least one parent who carries the mutations for FAD stands a high likelihood of developing the disease.
The genetic mutations behind FAD trigger the formation of unhealthy proteins. On chromosome 1, a mutation will skew presenilin 2; on chromosome 14, a mutation will lead to aberrant presenilin 1; on chromosome 21, a mutation will bring about the development of faulty amyloid precursor protein (APP). The preceding mutations diminish the body’s APP, which in turn leads to the development of amyloid plaque: the primary marker of FAD.
Late-onset Alzheimer’s is the far more common form of the disease, and it generally affects people over the age of 65. While there is no genetic mutation that is known to be at the root of most late-onset cases, the disease is believed to stem from a mix of habitual, environmental, and inborn factors.
The genetics of Alzheimer’s
Many researchers believe Alzheimer’s Disease is caused more by genetics than brain development. But, despite the lack of a direct gene correlation to the disease, the presence of apolipoprotein E (APOE) on chromosome 19 can increase the likelihood of Alzheimer’s developing in older adults. The variations of APOE are as follows:
- APOE ε4 – The most potent allele; not present in everyone, though an individual could have up to two APOE ε4 alleles, which would place that person at a higher risk for earlier onset of Alzheimer’s.
- APOE ε3 – The most common allele is also the most neutral since it has no bearing on whether a person does or doesn’t develop the disease.
- APOE ε2 – The rarest allele, which can actually make a person less likely to develop Alzheimer’s. Even if an individual with APOE ε2 does get the disease, it wouldn’t likely occur until much later in life.
The APOE ε4 allele carries the highest risk factor for Alzheimer’s, though not everyone with one or more APOE ε4 alleles develops the disease, and not everyone with Alzheimer’s has the allele.
Recent studies into the cause of Alzheimer’s have focused on regions in the genome, which encompasses an organism’s whole DNA. Through this research, doctors have isolated 33 genome regions as of 2015 that are believed to be relevant to the disease (“Alzheimer’s Disease Genetics”). With further development of two methods—one that examines the whole genome sequence; one that isolates the protein-coding parts of an individual’s genome—scientists hope to make discoveries on the biological gateways to diseases like Alzheimer’s and ultimately develop ways to intervene in the process.
In the meantime, an individual’s APOE alleles can be verified through a blood test; but due to the various factors that play into the disease, genetic testing will probably never arrive at a point of predicting a person’s likelihood for Alzheimer’s with complete certainty.
Alzheimer’s treatment and prevention
Studies into the effects of Alzheimer’s on populations throughout the world have led to theories on possible causation stemming from local environmental elements, as well as cultural and dietary factors. As of 2015, however, no applicable measures have been identified for the prevention of the disease. Despite the higher likelihood of AD development in people with histories of cardiovascular conditions like Type I and Type II diabetes, hypertension, and high cholesterol, statins—drugs used to treat the latter group of conditions—have proved ineffective at minimizing the symptoms of Alzheimer’s.
Though far from conclusive, research has indicated that non-steroidal anti-inflammatory drugs (NSAIDs) can lower the effects of amyloid plaques. This, in turn, has led to the assumption that NSAIDs can help reduce one’s risk of developing Alzheimer’s, though the drugs are not effective at treating the disease once in progress. Hormone therapy was administered in the past to select groups of postmenopausal women with hopes of treating dementia, but this proved ineffective and in some cases increased the risk (Marjoribanks et al.)
Lowering the risk of AD
By extension of the cognitive reserve theory—which holds that certain lifestyle practices reduce the probability of dementia—people who involve themselves in activities that exercise the mind are believed to run a lower risk of developing Alzheimer’s. Activities that fall under this category include reading, community activism, taking part in board games, and mastering musical instruments. Mastery of a foreign language, even among people past the age of 50, is also believed to lower the odds of AD and other forms of dementia.
An individual’s likelihood of developing Alzheimer’s could also hinge on his or her dietary choices. Diets believed to be in the low-risk category include Japanese and Mediterranean cuisine, as well as any basic diets low in fats and carbohydrates, such as most vegan, vegetarian, or pescatarian diets. The standard American diet—with its high volume of red meats, sugars, soft drinks, and frozen entrees—is believed to put people at a higher risk for AD and various other diseases.
For people who already have Alzheimer’s, the Mediterranean diet is believed to help with symptom-coping, because the diet’s emphasis on fruits, vegetables, legumes, olive oil, and low meat consumption provides cardiovascular benefits.
The exact dietary components that play into a person’s risk of AD development are less certain, due in part to the clashing results of various studies. There’s a small amount of evidence that foods and beverages rich in flavonoids—red wine, tea, dark chocolate—can lessen the threat of Alzheimer’s (Stoclet and Schini-Kerth). Research on the impact of vitamin C on the cognitive decline has found no relation, positive or negative (Heo et al.)
Todd, Stephen, et al. “Survival in dementia and predictors of mortality: a review.” International Journal of Geriatric Psychiatry 28.11 (November 2013): 1109–1124. Print.
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“Alzheimer’s Disease Genetics Fact Sheet.” National Institute on Ageing. U.S. Department of Health & Human Services. 16 Nov. 2015. Web. 18 Nov. 2015.
Marjoribanks, Jane; Cindy Farquhar; Helen Roberts; and Anne Lethaby. “Long term hormone therapy for perimenopausal and postmenopausal women.” Cochrane Library. John Wiley & Sons, Inc. 11 July 2012. Web. 19 Nov. 2015.
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