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Case study of an elderly person with Alzheimer's Disease £7.49
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  3. Goldsmiths, University Of London (GUL)
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  5. Applied Pathobiology

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Case study of an elderly person with Alzheimer's Disease

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A descriptive case study of an elderly women that shows symptoms and the GP decides to carry out a test (APOE Test). The document has a detailed explanation about clinical signs, outcome of APOE test and molecular pathways and mechanism associated with the disease, including the histopathology and...

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  • March 24, 2025
  • 5
  • 2023/2024
  • Case
  • Dr. nuñez
  • A

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Case 4

A)
The patient’s age and signs and symptoms were mentioned, with a positive result for
APOE E4. The provisional diagnosis is Alzheimer’s Disease, and the symptoms such
as memory loss, recognition of familiar faces and functional impairment are key
points for AD.
The dominant gene of Alzheimer’s is the apolipoprotein E (APOE) gene, which has
different alleles that influence the disease. APOE E3 is one of the common alleles
known to have a neutral effect on the disease, meaning that it is neither a risk nor a
prevention. This depends on other factors. Meanwhile, APOE E4 is an allele known
for its high risk for Alzheimer’s, most commonly carrying one copy, and about 2%-
5% carry two copies. (National Institute on Aging, 2023). APOE E2 allele protects
against AD, reducing amyloid plaque as APOE genotypes affect the formation of
amyloid- beta Aβ, causing plaques more commonly in carriers of APOE E4 allele and
neurofibrillary tangles (tau tangles), which are the pathological hallmarks of AD,
these tangles are formed from a neural microtubule linked protein present in axons.
In normal conditions, it is soluble and interacts with tubulin, encouraging the
formation of microtubules that aid the structure.


Models of AD have shown that overlapping processes, like inflammation, impaired
brain glucose metabolism and Aβ are more likely to be responsible for the unusual
hyperphosphorylation of tau. (Medeiros, Baglietto-Vargas and LaFerla, 2010)
Alterations in gene expression or activation of tau kinases and tau phosphatases are
frequently seen in AD patients. (Medeiros, Baglietto-Vargas and LaFerla, 2010)


The accumulation of Aβ plaques disrupts the synaptic function and causes neural
death, leading to the patient's symptoms, such as memory impairment as these
plaques activate microglia which are generally responsible for clearing debris and
helping neurons (Fruhwürth, Zetterberg and Paludan, 2024).

, Chronic inflammation results from the production of pro-inflammatory cytokines by
activated microglia, including interleukin -1β, the alpha form of tumour necrosis
factor, and interleukin-6. Initially, it is a protective reaction, but the response can turn
neurotoxic after persistent stimuli, resulting in synaptic dysfunction and neural death.
(Kinney et al., 2018) Astrocytes which are a kind of glial cells that are stimulated in
AD changes the blood-brain barrier and disrupting neural-glial connections also
contributing to neurodegeneration and releasing inflammatory molecules. (Kinney et
al., 2018)


The imbalance of different neurotransmitters, such as glutamate, acetylcholine,
dopamine, and serotonin, are responsible for the neurological changes seen in AD
patients. Acetylcholine (ACh) neurotransmitter is essential for memory and learning;
the levels of Ach decrease both in concentration and function in patients with AD.




B)
The APOE test uses patient’s DNA to define what combination of APOE gene is
present, so any other type of dementia can differentiate. APOE e3 is the most
common but APOE e4 allele confirms a high risk of Alzheimer’s disease. Having a
heterozygous copy of the e4 allele increases the risk of AD while having a
homozygous increase the risk even more; however, it is essential to keep in mind
that the presence of allele e4 does not mean the person will develop Alzheimer's
disease (Strittmatter and Roses, 1996), there's more factor included such as age and
lifestyle. The brain lipoproteins deliver cholesterol and essential lipids to neurons to
support synapses via receptors; lipoprotein-receptor protein (LRP), specifically LRP1
forebrain knockout (LRP1-KO) have decreased brain cholesterol, cerebroside and
dendritic and branching produced fewer synapses and causes neuroinflammation
and eventually neurodegeneration in AD patients, proving memory deficit and lack of
movement coordination caused by reduced synaptic functions.

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