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The issues covered in this weeks discussion will include the pathophysiology of Alzheimers disease (AD), particularly, the tools that junior and senior students can use to educate patients on the subject matter. By the end of the session, the audience will be capable of:
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Providing the target population with the essential information about the identification of AD symptoms;
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Educating patients about pathophysiology with the help of visual aids;
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Teaching patients to recognize the symptoms and choose the appropriate resources for managing the problem;
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Understanding the role of media in learning new information about AD and its treatment options.
Handout
Alzheimers disease is a type of multifarious neurodegenerative disease that progresses consistently as the patient experiences neuronal loss (Norton, Matthews, Barnes, Yaffe, & Brayne, 2014). According to the Alzheimers Association (2016), 13.8 billion people in the U.S. suffer from the disorder. Furthermore, the death toll has been increasingly high, as shown in Figure 1. The disease occurs at both intra- and extracellular levels. The former is characterized by the development of the neurofibrillary tangles, whereas the latter implies the development of amyloidal protein deposits. Each of the phenomena triggers the further creation of senile plaques (Norton et al., 2014).
There are currently several hypotheses about the pathophysiology of AD. However, one of the hypotheses is viewed as more credible than others. Defined as the ‘² hypothesis, the identified supposition implies that ‘² oligomers trigger the development of synaptic impairment and, therefore, affect the functioning of the brain (McCance, Huether, Brashers, & Rote, 2014). Amyloid plaques, in turn, are developed at the later stages of the AD progression, as the theory states.
The theory implies that the amyloid precursor protein (APP) should be split by - secretase, whereas the processing thereof should be carried out with the help of the ²- and ³-secretase. Thus, ‘² peptide production is enhanced, and the amount thereof exceeds the norm. Consequently, soluble oligomers are formed, causing the appearance of the beta-sheet conformation. The results of the identified process can be deemed as detrimental to the neurons of the human brain and include the following possible outcomes: oxidative damage, tau hyperphosphorylation, as well as synapses and mitochondria intoxication. As a result, the rapid process of brain degeneration is launched immediately as neurons start disintegrating, as shown in Figure 2 (Kumar & Ekavali, 2014).
Therefore, the accumulation of ‘² plaques is currently viewed as the primary factor causing the development of AD in patients. It should be noted, though, that the recent researches of chronic brain injury and ischemia show that A² should be viewed as a nonspecific marker of brain damage (McCance et al., 2014). As shown in Figure 1, the A² depositions are not linked specifically to the issue of AD. Therefore, the development of neurofibrillary tangles in the patients brain can be deemed as the area that needs further studies.
That being said, there is a range of evidence supporting the identified theory. For instance, a recent study showed that APP ectodomain serves as a ligand for the TNFRSF21 protein, also known as the Death Receptor 6 (DR6) (). In other words, deprived of the opportunity to grow, APP is caused to develop a cleavage that contributes to the release of the ectodomain that produces caspases 3 and 6, therefore, leading to the production of the DR6 protein. Consequently, the plaques are produced, and dementia (AD) progresses, as shown in Figure 3 above.
Evaluation of AD
To determine the development of AD, a nurse must examine the patients medical history thoroughly. Furthermore, the tests of the patients mental status and mood will have to be carried out, followed by a medical and physiological examination.
Treatment
The treatment options include cholinesterase inhibitors of memory loss and interventions aimed at reducing anxiety and depression. The management of changes in patients sleep patterns is also encouraged.
Video Summary
The Osmosis channel (2016) offers a very useful video that can shed a lot of light on the pathophysiology of AD. In their video, the owners of the Osmosis channel (2016) explain the concept of Alzheimers disease in great detail, yet rather simply. The narrator details how beta-amyloid plaque is collected in the human brain and, therefore, leads to neurofibrillary tangles in the brain. As a result, the atrophy of the brain begins, followed by symptoms such as memory deterioration. The video can be used as a perfect example of how the pathophysiology of Alzheimers disease can be explained to patients, thus, cultivating awareness among the target population. When coupled with visual aids, the said lecture helps get a deep insight into the nature of the disease and its pathophysiology.
Collapse
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Alzheimers Disease. AD is rapidly progressing dementia that is caused by a split of APP and the further development of amyloid plaques in the patients brain.
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Signs and symptoms. Memory loss, problem-solving skills deterioration, inability to perform routine actions.
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Pathophysiology. Development of beta-amyloid plaques in the patients brain.
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Evaluation. Study of the patients medical records, physiological and psychological examination.
Terms
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Neurofibrillary tangles tau protein aggregates.
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Amyloidal protein deposits teh aggregates triggering the structure entanglements.
References
Alzheimers Association. (2016). 2016 Alzheimers disease facts and figures. Alzheimers & Dementia: The Journal of the Alzheimers Association, 12(4), 459-509.
Eikelenboom, P., Hoozemans, J. J. M., Veerhuis. R., Exel, E. V., Rozemuller. A. J. M., & Gool, W. A. V. (2012). Whether, when and how chronic inflammation increases the risk of developing late-onset Alzheimers disease. Research & Therapy, 4(1), 15-23.
Kumar, A., & Ekavali, A. S. (2014). A review on Alzheimers disease pathophysiology and its management: An update. Pharmacological Reports, 67(2),195-203.
McCance, K. L., Huether, S. E., Brashers, V. L., & Rote, N. (2014). Pathophysiology: The biologic basis for disease in adults and children (7th ed.). Maryland Heights, MO: Mosby Elsevier.
Norton, S., Matthews, F. E., Barnes, D., Yaffe, K., & Brayne, C. (2014). Potential for primary prevention of Alzheimers disease: An analysis of population-based data. Lancet Neurology, 13(8), 788-794.
Osmosis channel. (2016). Alzheimers disease Plaques, tangles, causes, symptoms & pathology. YouTube.
Sindi, S., Mangialasche, F., & Kivipelto, M. (2015). Advances in the prevention of Alzheimers disease. F1000Prime Reports, 7(1), 50-61. doi:10.12703/P7-50.
Some key players in the pathogenesis of AD. (2012).
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