Alzheimer’s Disease as a Neurological Disease

Introduction to the Disease

History

Alzheimer’s 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, Alzheimer’s disease remains an untreatable condition. Nonetheless, several strategies for containing its effects have to be considered when addressing the needs of patients with Alzheimer’s.

Signs and Symptoms

Spotting Alzheimer’s 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 Alzheimer’s 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 Alzheimer’s disease.

Epidemiology

Being significantly underresearched, Alzheimer’s 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 Alzheimer’s 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 Alzheimer’s 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 Alzheimer’s.

Normal Anatomy and Physiology

Cell and tissue populations involved

Considering the cellular basis of Alzheimer’s, 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 Alzheimer’s, 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 one’s long- and short-term memory to produce crucial information.

Organs

Since Alzheimer’s disease affects primarily the brain of a patient, focusing on the specified organ appears to be reasonable. Before the onset of Alzheimer’s, a patient’s 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 Alzheimer’s disease do not occur.

Primary Functions

Before the development of Alzheimer’s, 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 Alzheimer’s disease.

Connections to Other Body Systems

Alzheimer’s 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 one’s movements, hence the relation of the disease to the musculoskeletal system (Braak & Del Tredici, 2020). Nonetheless, Alzheimer’s disease is functionally linked primarily to the nervous system.

Changes to the Anatomy and Physiology

Pathophysiology

As emphasized above, the changes that Alzheimer’s disease causes to the patient’s 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 patient’s 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 Alzheimer’s pathophysiology.

Treatment/Prevention Options

As established previously, there are presently no treatment methods that allow curing Alzheimer’s 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 Alzheimer’s are restricted to the medicine used for slowing down the pace of Alzheimer’s development and the tools for training the patients’ memory (Lawlor et al., 2018). Specifically, people with Alzheimer’s 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 Alzheimer’s 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 Alzheimer’s disease such as Namenda is very restricted. In addition, the available medication should also reduce the effects of other manifestations of Alzheimer’s, such as the loss of the ability to use spatial directions. By exploring the problem of Alzheimer’s further and seeking new forms of treatment, one will be able to advance the current framework for managing the needs of patients with Alzheimer’s.

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). Alzheimer’s 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 Alzheimer’s 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 Alzheimer’s 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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