Comprehensive Health Assignment: Alzheimer's Disease and Its Impact

This assignment provides a comprehensive overview of Alzheimer's disease, addressing its causes, symptoms, and diagnostic methods. The assignment details the role of the Golgi apparatus in the development of Alzheimer's disease and distinguishes between early-onset and late-onset forms. It also discusses the prevalence of the disease across different age groups and geographic locations, using graphs to illustrate the increasing risk with age. The assignment further explores the symptoms associated with the mild, moderate, and severe stages of Alzheimer's disease, along with the diagnostic procedures healthcare professionals employ. Prognosis, treatment options including cholinesterase inhibitors and memantine, and current research are also discussed, with a conclusion summarizing the impact of the amyloid precursor protein on mitochondrial function and energy production in affected cells. The assignment references several studies and research papers to support the information provided.

Running head: HEALTH
Student name
Student No
Unit
Title: Alzheimer's disease

HEALTH
Qn1.
According to the University of Pennsylvania (2013) the Golgi apparatus is a cell
organelle used to sort, translate and to traffic membrane and secretory proteins. Study on the
dysfunction of the Golgi apparatus such as phosphorylation of the Golgi stacking protein
leads to Golgi fragmentation. Changed Golgi structure together with neurons affects the
sorting, trafficking and processing of crucial proteins in sensory system. Therefore defects of
the Golgi apparatus leads to development of Alzheimer’s disease (AD) (Joshi, Bekier and
Wang, 2015).
Neuron Golgi apparatus (Joshi et al. 2015)
Qn.2. Alzheimer's disease is also known as Alzheimer’s. The disease was named after
Dr. Alois Alzheimer who discovered something unusual with the brain tissue of who had died
out of an abnormal mental disease. This was back in 1906.
Alzheimer’s disease (AD) is the leading cause of dementia among the elderly in the
world (Theriault, El Ali and Rivest, 2015). It is characterized by continued memory loss and
cognitive functions. Alzheimer’s is a progressive and irreversible brain disorder that destroys
one’s memory, ability to think and eventually one is unable to do their day to day activities. It
is most prevalent among the elderly aged above 60 years (National Institute of Aging, 2018).

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Qn.3 Alzheimer's disease is divided in to two depending on the age of onset; early
onset Alzheimer's disease (EOAD) and late onset Alzheimer's disease (LOAD). The early
onset Alzheimer's disease accounts for between 1 and 6 percent of Alzheimer's disease cases
and is prevalent among people aged between 30 and 65. The LOD affects people above 65
years. The apolipoprotein E (APOE) gene, which is in different forms, is associated with
LOAD, specifically the APOE ɛ4 gene. However, having this gene is not a guarantee one
would suffer from this disease, same as not having the gene. Researchers have also identified
regions of genome which increase the risk of the disease. The EOAD is as a result of
inherited changes in one of three genes (Bekris, Yu, Bird and Tsuang, 2010). It can also be
divided into mild, moderate and severe Alzheimer's disease.
Qn.4. The graphs below show the annual incident rate of AD per 100 people and its
prevalence in Europe according to Alzheimer's Association (2018)
Australia
Asia Pacific
Oceania
Asia E
Asia S
Asia SE
Asia Cent.
Europe W
Europe Cent
Europe E
America N.
Caribbean
Latin America
N. Africa
SSA W
SSA E
SSA Cent
SSA S
0
1
2
3
4
5
6
7
8
9
standardised prevalence (%)
standardised prevalence (%)
65-69 70-74 75-79 80-84 85+
0
1
2
3
4
5
6
7
8 Annual Alzheimer's disease incidents per 100
people
Age

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According to these graphs, Alzheimer's disease risk increases with increase in age. It
is also evident that America is leading in Alzheimer's disease cases.
Qn.5. symptoms of AD
The first symptoms of this disease vary from person to another. Some show signs
impaired cognitive activities such as memory problems (a condition called mild cognitive
impairment, MCI). MCI is also associated with movement difficulties and issues with sense
of smell. Others show non-memory aspects like word finding, spatial and vision problems
and impaired judgment and reasoning. During the mild stage one experiences difficulties in
handling money and paying bills, change of moods and personality, too much anxiety,
repeating questions and speech misplacing and losing things. At its moderate stage, one has
short attention span, difficulties organize thoughts and have a logical thinking, one is unable
to learn new thing, increased confusion and loss of memory, one is unable to recognize
family, hallucinations, outbursts of anger, restlessness, impulsive behaviours and repetition of
statements. At the severe stage one is unable to communicate, experiences seizures, weight
loss, lose bladed control. Increase sleep. Skin infections, groaning and difficulties in
swallowing (Mayeux and Stem, 2012). As the disease advances, its effect on the patient and
to the environment increases. It affects the person’s physical functioning. Some other effects
include pneumonia, bedsores, fractures, dehydration, inhaling food and fluid in to the lungs
and malnutrition.
Qn.6. Diagnosis
Health care professionals carry out different diagnostic methods to determine in a
person with memory loss is suffering from Alzheimer's dementia as dementia has other
causes. They also could carry out memory, attention, language, counting and problem solving
tests (Pistollato et al. 2016). Other standard tests could be carried out to determine any other

HEALTH
probable causes of the condition. For certainty and coming to a conclusion about the cause
the nurses carry out brain scans. These could be positron emission tomography, CT scan and
resonance imaging.
Qn.7, Prognosis
Each stage of Alzheimer's disease lasts for 2 years though some people take long in
the early stages and others shorter time. People suffering from Alzheimer's disease live for
about 10 years, though according to Qui, Kivipelto and von Strauss (2009) this depends on
the patient’s age as there are patients as young as 3 years. People suffering from this infection
are limited in conducting their activities and also cannot make their own decisions. They need
carers to be around them all the time.
Qn8. Ways of treating AD
Researchers and scientists have not discovered a cure for this disease according to
Barrack (2012) though research on treatment are ongoing. One is prescribed with
cholinesterase inhibitors and memantine. Cholinesterase inhibitors boost cell communication
by protecting a certain chemical messenger which is corrupted by this disease in the brain.
Qn9. Current research
Many researcher claimed that smoking could be a risk factor for AD but a recent
research by Abner et al. (2019) shows no relationship between the two. Research by Feng et
al (2019) discovered that eating mushrooms could reduce chances of cognitive impairment.
Current much research f focusing on coming up with a cure for this disease. The first drug to
be used for AD treatment was the tacrine approved in the 20th century (Asamoah, and Iyer,
2017).

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Qn.10. Conclusion
According to the University of Pennsylvania (2013) the amyloid precursor protein
(APP) moves from the cell nucleus, then directed to mitochondria. APP contains acidic
regions with negative charges which makes it to jam when moving mitochondrial membrane
protein transportation channels. This makes the mitochondria unable to obtain proteins and
manufacture energy.

HEALTH
References
Abner, E. L., Nelson, P. T., Jicha, G. A., Cooper, G. E., Fardo, D. W., Schmitt, F. A. and
Kryscio, R. J. 2019. Tobacco Smoking and Dementia in a Kentucky Cohort: A
Competing Risk Analysis. J Alzheimers Dis 68 (2). doi: 10.3233/JAD-181119.
Asamoah, B. O and Iyer, I. C. (2017). Alzheimer’s disease- The past, the present and the
future. Science Journal of Clinical Medicine. Vol. 6, No. 1, 2017, pp. 1-19. doi:
10.11648/j.sjcm.20170601.11
Alzheimer’s Association. 2018. Alzheimer’s Disease Facts and Figures. The Alzheimer’s
Dement, 14(3): 367-429.
Barrack, S. 2012. Advances in research and treatment for Alzheimer’s disease. New York:
International Medical Publishing.
Bekris, L. M., Yu, C. E., Bird, T. D., & Tsuang, D. W. (2010). Genetics of Alzheimer
disease. Journal of geriatric psychiatry and neurology, 23(4), 213–227.
doi:10.1177/0891988710383571
Feng, L., Cheah, K. M., Ng, M. X., Li, J., Chan, Y., Lim, S. L., Mahendran, R., Kua, E. H.
and Halliwe, B. 2019. The Association between Mushroom Consumption and Mild
Cognitive Impairment: A Community-Based Cross-Sectional Study in Singapore.
Journal of Alzheimer’s disease, Vol. 68, No. 1. Doi: 10.3233/JAD-180959
Joshi, G., Bekier, M. E., 2nd, & Wang, Y. (2015). Golgi fragmentation in Alzheimer's
disease. Frontiers in neuroscience, 9, 340. doi:10.3389/fnins.2015.00340
Mayeux, R., & Stern, Y. (2012). Epidemiology of Alzheimer disease. Cold Spring Harbor
perspectives in medicine, 2(8), 10.1101/cshperspect.a006239 a006239.
doi:10.1101/cshperspect.a006239

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National Institute of Aging. 2018. Alzheimer’s disease fact sheet. Retrieved from:
https://www.nia.nih.gov/health/alzheimers-disease-fact-sheet#changes
Pistollato, F., Ohayon, E. L., Lam, A., Langley, G. R., Novak, T. J., Pamies, D. and
Chandrasekera, P. C. (2016). Alzheimer disease research in the 21st century: past and
current failures, new perspectives and funding priorities. Oncotarget, 7(26), 38999–
39016. doi:10.18632/oncotarget.9175
Qiu, C., Kivipelto, M., & von Strauss, E. (2009). Epidemiology of Alzheimer's disease:
occurrence, determinants, and strategies toward intervention. Dialogues in clinical
neuroscience, 11(2), 111–128.
The University of Pennsylvania. (2013). Alzheimer's protein jams mitochondria of affected
cells; resulting 'energy crisis' kills neurons. Retrieved from:
https://www.eurekalert.org/pub_releases/2003-04/uop-apj040803.php
Thériault, P., ElAli, A., & Rivest, S. (2015). The dynamics of monocytes and microglia in
Alzheimer's disease. Alzheimer's research & therapy, 7(1), 41. doi:10.1186/s13195-
015-0125-2