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Introduction to the Disease
History
Alzheimers disease is a rather common condition in aging patients. Progressing at a moderate pace affects their nervous system and cognitive abilities significantly. The disease was discovered by Dr. Alois Alzheimer in 1906 (Prasad, 2020). Despite the time passed since its identification and recognition as a medical issue, Alzheimers disease remains an untreatable condition. Nonetheless, several strategies for containing its effects have to be considered when addressing the needs of patients with Alzheimers.
Signs and Symptoms
Spotting Alzheimers disease at an early stage is quite a challenge due to its gradual development. However, there are certain signs and symptoms to be aware of when addressing the needs of groups predisposed to the development of the disorder. The deterioration of short-term memory and the inability to retain information for certain amounts of time can be seen as the main warning sign of progressing Alzheimers disease (Van De Haar et al., 2016). The loss of problem-solving skills, spatial orientation abilities, and the propensity toward misplacing objects can be regarded as the primary signs of Alzheimers disease.
Epidemiology
Being significantly underresearched, Alzheimers disease has rather complicated epidemiology. The current distribution rates of the disease in Georgia are quite high, particularly, among representatives of the aging population (Haines, 2018). Specifically, around 120,000 Georgians are estimated to have Alzheimers disease or a related disorder (Georgia Department of Public Health, 2020). However, the key determinants of the disorder remain largely unknown. It is hypothesized that the abnormal accumulation of proteins and the development of plaque deposits within and close to brain cells is responsible for the development of Alzheimers disease (Haines, 2018). The described phenomenon causes the obstruction of neurons transmission and the development of axons (Bulgart et al., 2020). However, the specified hypothesis is yet to be confirmed as the main factor behind the development of Alzheimers.
Normal Anatomy and Physiology
Cell and tissue populations involved
Considering the cellular basis of Alzheimers, one will need to concentrate on the changes within the brain tissue. In patients with normal anatomy and physiology that have not been affected by Alzheimers, the nerve cell and tissue populations involved do not die at an unnatural pace (Pearson et al., 2020). Quite the contrary, the process of tissue regeneration and the development of nerve cells occurs at a reasonable pace, allowing the neuronal processes occurring within a brain to be structured accordingly. Thus, one can use ones long- and short-term memory to produce crucial information.
Organs
Since Alzheimers disease affects primarily the brain of a patient, focusing on the specified organ appears to be reasonable. Before the onset of Alzheimers, a patients brain has the regular anatomy and physiology, with no visible plaques obstructing the transfer of information within the synapses of the brain (Huang et al., 2016). Moreover, no accumulation of protein fragments that flow between the cells can be observed in the brain. Since nerve cells do not die in a healthy brain, the changes that lead to the development of Alzheimers disease do not occur.
Primary Functions
Before the development of Alzheimers, one is expected to have regular memory, namely, to be able to retain information and recall it whenever needed using short- and long-term memory. In addition, spatial coordination skills, as well as problem-solving abilities, are applied without noticeable challenges or complications. Finally, one should remember that speech and written communication occur naturally and effortlessly in patients before the development of Alzheimers disease.
Connections to Other Body Systems
Alzheimers disease is typically restricted to the nervous system of an individual and does not affect any other functions apart from the cognitive ones. However, due to the deterioration of spatial orientation skills, one may develop problems in coordinating ones movements, hence the relation of the disease to the musculoskeletal system (Braak & Del Tredici, 2020). Nonetheless, Alzheimers disease is functionally linked primarily to the nervous system.
Changes to the Anatomy and Physiology
Pathophysiology
As emphasized above, the changes that Alzheimers disease causes to the patients cognitive abilities and the nervous system are drastic in the long term. In the pathophysiological context, the development of plaques that obstruct the development and functioning of axons within a patients brain prevents essential processes within the nervous system to be implemented. Due to the development of beta-amyloid deposits outside brain cells and neurofibrillary tangles within cells, an individual experiences the loss of memory and other vital cognitive functions (Prasad, 2020). Thus, the misalignment of the primary protein in patients brains lies at the core of Alzheimers pathophysiology.
Treatment/Prevention Options
As established previously, there are presently no treatment methods that allow curing Alzheimers disease. Although experts are working on the problem, its solution will require detailed knowledge of brain functioning, which is currently unattainable. Therefore, the main treatment options for patients with Alzheimers are restricted to the medicine used for slowing down the pace of Alzheimers development and the tools for training the patients memory (Lawlor et al., 2018). Specifically, people with Alzheimers disease are typically prescribed cholinesterase inhibitors as the mechanisms that prevent further memory loss from happening.
At the same time, due to the lack of information about the specifics of Alzheimers disease development, the mechanisms of suppressing its symptoms and leading to its improvement are largely unknown. As a result, the efficacy of the medication that is currently available for treating Alzheimers disease such as Namenda is very restricted. In addition, the available medication should also reduce the effects of other manifestations of Alzheimers, such as the loss of the ability to use spatial directions. By exploring the problem of Alzheimers further and seeking new forms of treatment, one will be able to advance the current framework for managing the needs of patients with Alzheimers.
References
Braak, H., & Del Tredici, K. (2020). From the Entorhinal region via the prosubiculum to the dentate fascia: Alzheimer disease-related neurofibrillary changes in the temporal allocortex. Journal of Neuropathology & Experimental Neurology, 79(2), 163-175.
Bulgart, H. R., Neczypor, E. W., Wold, L. E., & Mackos, A. R. (2020). Microbial involvement in Alzheimer disease development and progression. Molecular Neurodegeneration, 15(1), 1-12.
Georgia Department of Public Health. (2020). Alzheimers disease.
Haines, J. L. (2018). Alzheimer disease: perspectives from epidemiology and genetics. The Journal of Law, Medicine & Ethics, 46(3), 694-698.
Huang, W. J., Zhang, X. I. A., & Chen, W. W. (2016). Role of oxidative stress in Alzheimers disease. Biomedical Reports, 4(5), 519-522.
Lawlor, B., Segurado, R., Kennelly, S., Olde Rikkert, M. G., Howard, R., Pasquier, F.,& & Coen, R. (2018). Nilvadipine in mild to moderate Alzheimer disease: A randomised controlled trial. PLoS Medicine, 15(9), 1-8.
Pearson, A., Ajoy, R., Crynen, G., Reed, J. M., Algamal, M., Mullan, M.,& Ojo, J. O. (2020). Molecular abnormalities in autopsied brain tissue from the inferior horn of the lateral ventricles of nonagenarians and Alzheimer disease patients. BMC Neurology, 20(1), 1-20.
Prasad, A. S. V. (2020). The essentials of biochemistry of the proteins as related to Alzheimers disease: A review. International Journal of Biochemistry Research & Review, 29(1), 34-49. Web.
Van De Haar, H. J., Burgmans, S., Jansen, J. F., Van Osch, M. J., Van Buchem, M. A., Muller, M.,& Backes, W. H. (2016). Blood-brain barrier leakage in patients with early Alzheimer disease. Radiology, 281(2), 527-535.
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