Comprehensive Case Study: Alzheimer's Disease, Symptoms, and Treatment

This case study examines a patient suffering from mild to moderate Alzheimer's disease, characterized by memory loss, confusion, and social withdrawal. The study delves into the pathophysiology of the disease, highlighting the roles of senile plaques, neurofibrillary tangles, and neuronal loss. It explores the connection between depression, social withdrawal, and the progression of Alzheimer's. The pharmacologic management section discusses the importance of slowing the decline rather than aiming for a cure, and it explores the use of acetylcholinesterase inhibitors like Donepezil, Rivastigimine, and Galantamine. The case study also touches upon the use of Vitamin E, Memantine, anti-inflammatory agents, and herbal supplements like ginkgo biloba. The study emphasizes the need for a comprehensive approach to manage the disease and improve the patient's quality of life, citing relevant research and studies to support the findings.

Running head: CASE STUDY ON ALZHEIMER’S DISEASE
CASE STUDY ON ALZHEIMER’S DISEASE
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Pathophysiology associated with disorder symptoms:
The patient is suffering form mild and moderate levels of Alzheimer’s diseases. He is having
memory loss and confusion. He is also having issues with recognition of family members and
friends and had withdrawn him socially. He is also suffering from depression and therefore
he is having a very low quality life. Alzheimer’s disease mainly affects three important
aspects that are helpful in keeping the neuron healthy (Da Mesquito et al., 2016). They are
the communication, metabolism as well as the repairs. There are many researchers who have
stated that these disorders mainly arise when the important nerve cells of the brain stop
working along with the losing of connections with other nerve cells ultimately resulting in
death. It the destruction as well as the death of the mentioned nerve cells which become
mainly responsible for the cause of memory failure, personality changes as well as problems
in leading the daily activities of life (Wood et al., 2015). Researchers are of the opinion that
the development of senile plaques precedes the onset of the disorder. Also the formation of
neurofibrillar tangles, neuron loss and also synapse loss take place in association of the main
progression of cognitive decline.
In normal cases, the protein called tau which is responsible in binding with the microtubules
of healthy neurons is responsible for stabilising the nerves. In case of the disorder, these tau
proteins chemically change and thereby pairs with other threads of tau forming different
tangles. These lead to formation of neurofibrillary tangles that affect the communication in
between the neurons. These ultimately cause cell death (Kumar & Singh, 2015). Also senile
plaques which are also called the beta-amyloidal plaques and cerebro-cortical atrophy at the
macroscopic level are also responsible for the sufferings of the patients.

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In case of Alzheimer’s patients plaques are mainly developed in the hippocampus which is a
structure deep in the brain. This part is mainly responsible in encoding memories. Plaques
also appear in other areas of cerebral cortex which mainly help an individual in thinking and
also in decision making. Therefore it is seen in the case study, that the individual is suffering
from memory loss symptoms largely. Tangles are also insoluble twisted fibres that build up
inside the nerve cells that hamper the memory system of patients.
A large number of studies have suggested that development of depression and also social
withdrawal increases the chance of getting affected by dementia and Alzheimer’s diseases by
many folds. Investigations which have been done by researchers show that depression is
intricately linked with Alzheimer’s, the exact biological background is still under controversy
but evidences available suggest that depressed people always produce hormone cortisol in
high levels. This has negative effect on the part of the brain responsible for new learning as
well as short term memory which is the hippocampus (Abolhassani et al., 2017). People like
the patient in the case study who are depressed have higher level of cortisol that mainly is
hormone related with stress response and also has a smaller hippocampus. Many others
suggest that depression causes chronic inflammatory changes which dispose depressed
patients to neurodegenerative disorders like Alzheimer’s disorder. As his own property was
getting g divides, it might have lead him to depression and social withdrawal which h had
caused him to suffer form Alzheimer’s as well.
Pharmacologic management:
The professional should keep in mind that Alzheimer’s diseases is a progressive diseases
where the patient will continue to decline in function whether they are rerated or are kept
without treatment. Therefore, pharmacologic management would be such that it would help
to preserve and facilitate the remaining function of the synapse and allowing a higher level of

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function for a longer time rather than making goals of stopping the neuronal loss (Carbera et
al., 2015). The later is simply not logical and will not bring any fruitful results. Slowing the
decline will be beneficial for the patients and although the management would not fully cure
him of the disorder but will help to slow down the process of degradation.
One of the best treatment paradigms would be to avail for the cholinergic benefits. If the loss
of acetylcholine is the main reason that results in defect of the primary neurotransmitter, then
increment in its production and at the same time inhibiting destruction and also activating the
receptors provide a beneficial therapy for slowing the decline (Wang et al., 2014). ACH
breaks down in the synaptic junctions by acetylcholinesterase. By this breakdown
prevention , medicines of this enzyme group can prevent destruction of ACH. Donepezil,
rivastigimine and galantamine are important acetyl cholinesterase inhibitors who work in the
same patterns. They have low incidence of serous reactions but they show various
cholinergic side effects. These include anorexia, vomiting, nausea, and diarrhoea; however
the patient develops tolerance to them over time. They help in improvement of cognition,
global impressions, functions, disturbed behaviours and others. Instruments that measure the
cognition power are the Mini-Mental State Examination, Alzheimer's disease Assessment
Scale, Cognitive Section, Neuropsychiatric Inventory, Physical Self-Maintenance Scale and
Instrumental Activities of Daily Living1 and others are also used (Varcolis et al. 2016).
Vitamin E is also believed to mitigate the inflammatory response of the plaque formation in
the brain.
Memantine is a recently approved drug by NMDA antagonist. They basically interfere
with the glutaminergic overstimulation causing excite-toxicity. By interfering with that of the
excite-toxicity it affects the receptors of NMDA that takes part in memory processing and
pathology of the disorder. The drug is found to be very effective in trials conducted by

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researchers and bring positive results in cognition, function and also in behaviour and global
status.
Pathology tests have showed that people who suffer from the disorders have microscopic
inflammation in their brain and as a result anti-inflammatory agents are found to be useful in
such a scenario. These often include diclofenac, rofecoxib, naproxen and also most recently
ibuprofen. However, there are not many evidences which suggest the continuance of the
medicines as protective agents for Alzheimer’s disorder.
Herbal supplements are also said to be helpful for this disorder when used in
conjunction of other prescribed therapies. The most frequent choice includes the use of ginko
biloba which mainly act as a flavoglycoside in its pharmacologic effect. This mainly acts a s
potent free radical scavenger and function as antioxidant.

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References:
Abolhassani, N., Leon, J., Sheng, Z., Oka, S., Hamasaki, H., Iwaki, T., & Nakabeppu, Y.
(2017). Molecular pathophysiology of impaired glucose metabolism, mitochondrial
dysfunction, and oxidative DNA damage in Alzheimer's disease brain. Mechanisms of
ageing and development, 161, 95-104.
Cabrera, E., Sutcliffe, C., Verbeek, H., Saks, K., Soto-Martin, M., Meyer, G., ... &
RightTimePlaceCare Consortium. (2015). Non-pharmacological interventions as a
best practice strategy in people with dementia living in nursing homes. A systematic
review. European Geriatric Medicine, 6(2), 134-150.
Constantin, G. (2016). ROLE OF PERIPHERAL INFLAMMATION IN COGNITIVE
IMPAIRMENT AND ALZHEIMER’S DISEASE. Alzheimer's & Dementia: The
Journal of the Alzheimer's Association, 12(7), P221.
Dá Mesquita, S., Ferreira, A. C., Sousa, J. C., Correia-Neves, M., Sousa, N., & Marques, F.
(2016). Insights on the pathophysiology of Alzheimer's disease: the crosstalk between
amyloid pathology, neuroinflammation and the peripheral immune
system. Neuroscience & Biobehavioral Reviews, 68, 547-562.
Kumar, A., & Singh, A. (2015). A review on Alzheimer's disease pathophysiology and its
management: an update. Pharmacological Reports, 67(2), 195-203.
Varcarolis, E. M. (2016). Essentials of Psychiatric Mental Health Nursing-E-Book: A
Communication Approach to Evidence-Based Care. Elsevier Health Sciences.
Wang, J., Yu, J. T., Wang, H. F., Meng, X. F., Wang, C., Tan, C. C., & Tan, L. (2014).
Pharmacological treatment of neuropsychiatric symptoms in Alzheimer9s disease: a
systematic review and meta-analysis. J Neurol Neurosurg Psychiatry, jnnp-2014.

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Wood, P. L., Medicherla, S., Sheikh, N., Terry, B., Phillipps, A., Kaye, J. A., ... & Woltjer, R.
L. (2015). Targeted lipidomics of fontal cortex and plasma diacylglycerols (DAG) in
mild cognitive impairment and Alzheimer’s disease: validation of DAG accumulation
early in the pathophysiology of Alzheimer’s disease. Journal of Alzheimer's
Disease, 48(2), 537-546.