Alzheimer’s Disease is a disease that affects the nervous system, specifically the brain. It is a disease that attacks the connective tissues in the brain, causing the tissue to die and affecting how the brain functions. The brain shrinks naturally with age, but typically does not lose a large number of neurons. In Alzheimer’s disease the neurons lose connections with other neurons; the connections are usually destroyed in parts of the brain that are used in memory function such as the hippocampus and the entorhinal cortex. The formation of amyloid plaques and neurofibrillary tangles are a cause to the degeneration of the neurons. The disease then wide spreads to the cerebral cortex, which is in control of speech, reasoning, learning and social behavior. Eventually a person with Alzheimer’s loses their ability to live independently. Because Alzheimer’s is a disease that cannot be cured, actions such as integrating more social contact and changing lifestyle patterns could delay the progression of the disease or even help prevent it.

Alzheimer’s disease takes place in the central nervous system (CNS), which contains the brain, spinal cord, and neurons. In the CNS, the brain is responsible for most of the sensory information and coordination in the body both conscious and unconscious. The brain takes on complex actions like thinking and feeling. There are two types of tissues in the brain, grey and white matter. Grey matter consists of the nerve cell bodies, dendrites and axons. The white matter mostly consists of axons. The hypothalamus is critical for homeostasis in the brain and the body’s internal environment. The cerebrum is responsible for the brains conscious sensations and voluntary movement and also functions like thinking, learning, problem solving and emotion (Newman, 2017). It is no wonder that the symptoms of Alzheimer’s disease affect memory and cognition.

Amyloid plaques are said to be a direct cause of neuron death. Amyloid is a term for the protein fragments that the body produces naturally. Alzheimer’s disease is the accumulation of these proteins between nerve cells, specifically the beta amyloid fragments. Normally the beta amyloids are broken down in a healthy brain, but in a diseased brain the pieces form together and create hard plaques that cannot

be broken down. Neurofibrillary tangles are hard twisted fibers found in the brain cells these tangles form a microtubule. In a healthy brain the microtubules help transport nutrients to other nerve cells, but in a brain with Alzheimer’s the microtubule structures are collapsed. It is not known if the formation of these plaques and neurofibrillary tangles are the earliest form of the disease process and their role in the direct

Normal Beta-amyloid vs. Alzheimer’s Beta-amyloid Kwon, D. (2018, July 24)

Cause of the disease is controversial (Hardy, 2013).

Oxidative stress causing neuroinflammation is thought to play a large role in a number of central nervous system disorders including Alzheimer’s. The microglia function is necessary for the brain’s homeostasis and the microglia show exaggerated responses to systemic inflammation, which impairs cognitive function (D’Avila, 2018). The Microglia are key in the brain’s immune system and are a first line of defense in neuronal insults (Suridjan, 2015). Neuroinflammation is thought to progress the disease by increasing the build up of beta amyloid plaques and causes the neurodegeneration of microglial activation. The release of these inflamed cytokines reduce the clearance of the beta amyloid plaques and increases its production (Alasmari, 2018). Tangle formations directly result in the deprivation of the hippocampus and the entorhinal cortex.


Aging is a natural process that affects the brain and cognitive decline as well as function and social impairments. It is normal to see decline in the hippocampal function in memory consolidation and also behavior and mood regulation. In fact, oxidative stress, neuroinflamation, altered intracellular signaling; reduced synaptic plasticity and altered gene expression are believed to be natural processes of the aging brain (Bettio, 2017). The hippocampus is a part of the brain the directly correlates with memory and when, in a diseased state, such as a brain with Alzheimer’s, the hippocampus is affected mostly in size. The hippocampus is located under the medial temporal lobes. The hippocampus’ job is to help us make new memories and be able to retrieve old memories in the long-term memory bank. Research shows that the hippocampus is one of the first areas affected by Alzheimer’s. The hippocampus shrinks and atrophies which causes the impairment of developing new memory and recalling old memory. Image analysis of the hippocampus has recently become an interest in diagnosing Alzheimer’s through MRIs. This allows professionals to see the hippocampal shapes and the symmetry and volume. Volumetric variations are one of the primary indicators in differentiating a healthy aging brain and a diseased brain (Suksuphew, 2017).

Healthy brain vs. shrinking brain in advanced Alzheimer’s disease. Alzheimer’s Brain. (2017).

The entorhinal cortex is located in the medial temporal lobe and is in charge of memory, navigation and perception of time, which can be damaged in the progression of Alzheimer’s disease. In recent studies the volume of the entorhinal cortex has been tested along side the size of the hippocampus in healthy aging adults and adults with early onset of Alzheimer’s disease. The results, through imaging, based on postmortem studies, concluded that the entorhinal cortex is the first site and location that the disease occurs and then moves on to the hippocampus. This study was conducted with patients with mild cognitive impairment and not all mildly impaired individuals have Alzheimer’s disease (Suksuphew, 2017). The destruction of the hippocampus and entorhinal cortex in the progressive disease is the cause of memory deficiency at higher rates than normal or healthy aging in the brain.

The general stages of Alzheimer’s disease can vary in different patients and can vary over the time period in which it progresses. The first 2-7 years are mild stages of the disease. In the first stage, there is usually no impairment and the patient seems to have normal cognition; typically other people don’t notice. Stage two has a mild cognitive decline such as forgetting words or misplacing things. Stage three consists of early confusion and mild impairment. This is usually when patients try to hide their symptoms; they cannot recall what was just said, and they have problems planning. Stage three is usually when the symptoms of Alzheimer’s starts to have an affect on daily living. Stage four is considered mild Alzheimer’s disease and lasts about 2 years. In these two years, financials and math start to become difficult and the ability to remember events or recall memories is a challenge. The patient may have issues performing tasks that require stages like cooking or driving. A diagnosis at this stage is usually accurate. Stage five is moderate Alzheimer’s disease. Cognitive decline becomes more drastic, the patient is more likely to become disoriented and need assistance. This is usually the stage where decision making and reasoning is affected. In stage six, the patient is considered to have moderately severe Alzheimer’s, where they have lack of awareness and ability to remember the past and cannot carry on a conversation. Basic daily tasks will be something that the patient will now need help in and remembering names of family members is rare. Stage seven is the final stage of progressive Alzheimer’s and it is considered sever. Speech becomes limited and even movement becomes limited and difficult because the disease has spread to those parts of the brain. Total assistance is necessary at this stage because the patient will no longer be able to discern when they are hungry and thirsty and no longer be able to carry out the daily living tasks. Not all patients will experience these stages in this timeline or even time period (Marshall, 2018).


Memory isn’t the only symptom of Alzheimer’s though; social behavior and social cognition are also impaired in the progression of the disease. Patients with Alzheimer’s disease are typically not able to socialize like a healthy aging person. They’re confused and less trusting and mood swings are a part of their disease. Being as it is that the cerebral cortex, which is directly affiliated with emotion, is affected in Alzheimer’s, it is not surprising that patients suffer social disabilities. In a recent study, twenty-seven patients with Alzheimer’s and their significant others were studied in their relationships and how the disease affects the interaction between the partners. Because patients with the disease have severe deficits with emotional processing and emotional recognition the relationships started to suffer causing changes in social behavior and being apathetic towards the other. Behavior changes such as apathy, and agitation in participants with dementia were significantly related to relationship continuing (Poveda, 2017).

Some studies have shown that social environment and social relationships can affect a patient’s behavior and mental health. There has been a study that analyzed the correlation between loneliness and the risk of developing Alzheimer’s disease and the progression of it as well. The study revealed that people who were lonely had higher risks of developing the disease compared to other people who were not lonely. It was also shown that the disease progression in cognitive decline could be prevented and even delays the onset of the disease if patients keep mentally active and frequently participate in social activities. Social isolation exasperates cognitive impairment and memory and also causes psychosocial stress, which in turn increased oxidative stress and inflammatory reactions in the brain. Social isolation aggravates Alzheimer’s associated memory decline (Hsiao, 2018).

Social isolation in Alzheimer’s disease. Institute. (2016, April 21).

Social interaction rescues Alzheimer patients’ memory by increasing Brain-derived neurotropic factor (BDNF). The BDNF increases synaptic plasticity and enhances cognitive function; it also decreased depressive episodes in patients (Hsiao, 2018). Clinicians and medical reports advise us that patients can reduce the cognitive rundown and delay the onset of the disease by maintaining strong social connections and frequent activities. An easy intervention to the memory decline in patients is to have daily meetings either with family members, or if in a facility, with members of the community. Doing activities such as card games or talking or listening to music in the company of other human beings can delay the progression of the disease.               Alzheimer’s disease inhibits the ability to communicate or participate in social interaction and as a consequence can cause a feeling of loneliness and isolation. Research as shown that constant isolation and social depression can cause hallucinatory experiences, which is a frequent happening in patients with the disease. To test this hypothesis that social isolation causes depression and hallucinations, a sample of twenty-two patients with mild Alzheimer’s and twenty-four healthy elderly participants were assessed using the Launay-Slade Hallucination Scale. The scale explores contact and social participation. The Results showed that more hallucinatory experiences and social isolation were found in the Alzheimer’s group as apposed to the healthy group of elders. The discussion following the study between researches suggested that the hallucinations were a mechanism to fulfill communication needs and escape a cycle of boredom (El Haj, 2016). Verbal play early on in the beginning stages of Alzheimer’s such as creative language to make puns, jokes, and rhymes could help maintain speech abilities as the disease progresses. Speech therapy throughout the disease could help prevent the impact of social isolation the disease leaves on the patient, which in turn could prevent or lower the hallucination rate (Shune, 2013).

Though a disease like Alzheimer’s is irrevocable, lifestyle interventions like diet and exercise have played a large role in the prevention and slowing of the progression. Specific dietary patterns such as the Mediterranean diet, which is based on the high consumption of omega-3 fatty acids and polyphenol-rich foods such as olive oil, nuts and vegetables and fruits has been associated with a reduced risk in cognitive decline. In Japan, Alzheimer’s has greatly increased due to the incorporation of the western diet as compared to the normal diet of fish and vegetables. To test these outcomes, two pilot studies have reported outcomes from individual lifestyle interventions consisting of high nutrient and low carbohydrate diets, resulting in a reduction of the Alzheimer’s symptoms based on neuropsychological tests and neuroimaging (D’Cunha, 2017).

Another aspect of nutrition is micronutrients. Research has shown that micronutrients such as a vitamin B-12, vitamin D and folic acid are pivotal in brain function and mental and emotional health as adult’s age. In a cross sectional study done with adults age 60-75 over 17 months, proved that the deficiency in these vitamins have a positive correlation in the serum evaluated in the study in patients with senile dementia of Alzheimer’s Type. One hundred and ten patients suffering from the disease were evaluated. Two groups were studied. One group of 110 patients was given the supplements and another group of 55 patients were given a placebo. The results in the serum were higher by average in the group given the supplementation by 23% as compared to the control group. The study concluded that adults who were deficient in vitamin D, vitamin B-12, and folic acid were at higher risk of senile dementia of Alzheimer’s type than those who supplemented the vitamins (Vashistha, 2018). Adding simple supplementation of vitamins and micronutrients is an easy way to prevent Alzheimer’s disease, enhance brain function and help aid healthy aging in the brain.

Not only is diet and micronutrients an important to nutrition when it comes to nuerodegenerating disease like Alzheimer’s, but also implementing calorie restriction. In laboratory animals, such as rats, calorie restriction was proven to protect against aging, oxidative stress, and neurodegenerative pathologies. Reduced levels of growth hormone, which mediate some of the positive effects of a calorie restricted diet, can also extend longevity and protect against the neurodegenerative diseases in the rodents and even humans. Severely restricted diets were difficult to maintain and are associated with chronic low weight and major side effects such as bone mass decreasing. The study with laboratory rodents showed four months of periodic protein restriction and supplementing essential amino acids showed significant cognitive improvement with the mice already displaying impairment. This study showed that implementing a protein restricted diet on cycles would protect against age-related neuropathology (Parrella, 2013). Reducing the amount of meat a person intakes drastically changes the amount of calories put into the body. There are not many interventions that have been proven to significantly change results incurred with Alzheimer’s, except for calorie restriction and exercise.


There have been numerous large cohort studies that have been conducted that indicated that physical activity or exercise could enhance cognitive function and delay the onset of Alzheimer’s disease and other dementias. Preventative strategies have been the only way to help the disease since a cure has not been found. Therapeutic trials focusing on the effects of physical activity and exercise and how the factors are associated with healthy brain aging is a way to investigate these preventative strategies. The evidence from the epidemiological studies have found better reaction time in older men who participate in racket sports, such as tennis or running compared to men who have sedentary lifestyles. Verbal memory, executive functioning and attention were all categories that active aging men scored higher in. There have not been any follow up studies on whether the amount of physical activity and exercise is correlated with the amount of cognitive domains; however, in contradiction to the theory that the amount of time does not correlate to the domains in cognition, a study that used an exercise questionnaire on 1324 subjects and it was found that light, not vigorous exercise at mid- life to late-life was associated with reduced risk of memory impairment (Brown, 2013).

Senior Fitness: A Key to Healthy Aging. (2013, November 25)

In a study that supervised the aerobic activity on an exercise program over six months, 68 individuals with early onset of Alzheimer’s were tested to see if their cognition improved. The study was randomized and monitored by trained exercise specialists. The program consisted of 150 minutes of aerobic exercise a week versus non-aerobic stretching and toning control intervention. Neuropsychological tests were conducted at the start, the thirteenth week and the final week to access memory and functional ability and depressive symptoms. The aerobic exercise was associated with a slight gain in functional ability compared to the group that did non-aerobic activity and analyses revealed that enhancing cardiorespiratory fitness positively correlated with memory performance and hippocampus volume. The conclusion of this study was that cardiovascular exercise might be an important key in brain benefits and reduced hippocampal atrophy (Morris, 2017).

Based on research and findings with exercise and Alzheimer’s disease, a healthy intervention with early onset Alzheimer’s is to take up a passive sport for recreation or to introduce cardiovascular exercise as a part of daily routine. Depending on age and ability to move, walking briskly everyday for twenty- five minutes could also be a great way to supplement for exercise. In the later stages of Alzheimer’s walking may be the only physical activity a patient can take on. It takes activity in the brain to make functional movement or any physical activity at all, which could suggest why activity improves verbal memory, executive functioning and attention.

In conclusion, Alzheimer’s disease is incurable. It affects the regions of the brain such as the entohrinal cortex, the cerebral cortex (temporal lobes) and the hippocampus. The main findings and diagnosis are based on size and atrophy of these areas. Another root cause to the disease is the beta-amyloid protein plaques building up and blocking nerve cells in the brain and causing them to die off. Alzheimer’s is a disease affects people at different rates and progresses in patients uniquely. The disease has affected more people presently than ever in the past due to the longevity of age now; its rapid incline in the population has left health experts with no choice but to find a cure. It leaves patients and peoples no choice, but to be proactive and implement interventions into their daily living. In the researched findings, the earlier an individual changed their lifestyle behavior, the less likely they were to experience cognitive decline early on. Social behavior is a major debilitation in the disease and can be taken into account in preventative way such as joining a social group and aging alongside people of the same age as well as setting up patient’s with Alzheimer’s with a group of people on a regular basis and implementing a speech therapist. Changing lifestyle such as diet and exercise are great ways to age healthily and take care of the brain by giving it proper nutrients and oxygen.


Works Cited

  • Alasmari, F., Alshammari, M. A., Alasmari, A. F., Alanazi, W. A., & Alhazzani, K. (2018). Neuroinflammatory cytokines induce amyloid beta neurotoxicity through modulating amyloid precursor protein levels/metabolism.

    BioMed Research International, 2018

    , 1-8.
  • Alzheimer’s Brain. (2017). Retrieved December 9, 2018, from https://www.keepmemoryalive.org/brain-science/alzheimers-brain
  • Bettio, L. E. (2017). The effects of aging in the hippocampus and cognitive decline.

    Neuroscience & Biobehavioral Reviews.,79

    , 66-82. Retrieved December 9, 2018.
  • Brown, B. M., Peiffer, J. J., & Martins, R. N. (2013). Multiple effects of physical activity on molecular and cognitive signs of brain aging: Can exercise slow neurodegeneration and delay Alzheimer’s disease?

    Molecular Psychiatry,18

    (8), 864-874.
  • D’Avila, J. C., Siqueira, L. D., Mazeraud, A., Azevedo, E. P., Foguel, D., Castro-Faria-Neto, H. C., . . . Bozza, F. A. (2018). Age-related cognitive impairment is associated with long-term neuroinflammation and oxidative stress in a mouse model of episodic systemic inflammation.

    Journal of Neuroinflammation,15

    (1).
  • D’Cunha, N. M., Mckune, A. J., Panagiotakos, D. B., Georgousopoulou, E. N., Thomas, J., Mellor, D. D., & Naumovski, N. (2017). Evaluation of dietary and lifestyle changes as modifiers of S100β levels in Alzheimer’s disease.

    Nutritional Neuroscience,22

    (1), 1-18.
  • El Haj, M. (2016). Hallucinations, loneliness, and social isolation in Alzheimer’s disease.

    Cognitive Neuropsychiatry.,21

    (1), 1-13. Retrieved December 9, 2018.
  • Hardy, J., & Higgins, G. (2013, April 10). Alzheimer’s disease: The amyloid cascade hypothesis. Retrieved December 8, 2018
  • Hsiao, Y., Chang, C., & Gean, P. (2018). Impact of social relationships on Alzheimer’s memory impairment: Mechanistic studies.

    Journal of Biomedical Science,25

    (1).
  • Institute. (2016, April 21). Why senior socialization is critical to your loved one’s health. Retrieved December 9, 2018, from https://blog.ioaging.org/caregiving/senior-socialization-critical-loved-ones-health/
  • Kwon, D. (2018, July 24). Dutch university hospital halts amyloid beta drug studies. Retrieved December 9, 2018, from https://labiotech.eu/medical/amyloid-beta-halt-alzheimers/
  • Marshall, T. (2018). Stages of dementia and Alzheimer’s disease. Retrieved December 8, 2018
  • Morris, J. K., & Vindoni, E. D. (2017). Aerobic exercise for Alzheimer’s disease: A randomized controlled pilot trial.

    PLoS ONE.,2

    (12), 1-14. Retrieved December 9, 2018.
  • Newman, T. (2017, December 22). Central nervous system: structure, function, and diseases. Retrieved December 8, 2018
  • Parrella, E., Maxim, T., Maialetti, F., Zhang, L., Wan, J., Wei, M., . . . Longo, V. D. (2013). Protein restriction cycles reduce IGF-1 and phosphorylated Tau, and improve behavioral performance in an Alzheimers disease mouse model.

    Aging Cell,12

    (2), 257-268.
  • Poveda, B., Osborne-Crowley, K., Laidlaw, K., Macleod, F., & Power, K. (2017). Social cognition, behavior and relationship continuity in dementia of the Alzheimer type.

    Brain Impairment,18

    (02), 175-187.
  • Senior fitness: a key to healthy aging. (2013, November 25). Retrieved December 9, 2018, from https://maineseniorguide.com/senior-fitness-a-key-to-healthy-aging/
  • Shune, S., & Duff, M. C. (2013). Verbal play as an interactional discourse resource in early stage Alzheimers disease.

    Aphasiology,26

    (6), 811-825.
  • Suksuphew, S., & Horkaew, P. (2017). Hyperplanar morphological clustering of a hippocampus by using volumetric computerized tomography in early Alzheimer’s disease.

    Brain Sciences,7

    (12), 155.
  • Suridjan, I. (2015). In-vivo imaging of grey and white matter neuroinflammation in Alzheimer’s disease: A positron emission tomography study with a novel radioligand, [18F]-FEPPA.

    Molecular Psychiatry,

    1579-1587. Retrieved December 8, 2018.
  • Vashistha, P., Zahra, K., Kumar, A., Kumar, T., Srivastava, M., & Mishra, S. P. (2018). Is there a correlation between micronutrients and cognitive status: an exploratory study of senile dementia of alzheimer’s type.

    Journal Of Clinical And Diagnostic Research

    .


 

PLACE THIS ORDER OR A SIMILAR ORDER WITH NURSING TERM PAPERS TODAY AND GET AN AMAZING DISCOUNT

get-your-custom-paper
CategoryUncategorized

For order inquiries     +1 (408) 800 3377

Open chat
You can now contact our live agent via Whatsapp! via +1 408 800-3377

You will get plagiarism free custom written paper ready for submission to your Blackboard.