This is the first submission for this project. Please select an alteration in health (disease) that you would like to work on. Be sure to select a disease that has enough information and depth to meet the project requirements. Describe the selection in one paragraph and why you chose it. You may use your textbook or other resources for your selection. The disease selected must be approved by your instructor before you continue on to the next project assignment.

One disease that I have chosen to work on is Alzheimer’s disease. Alzheimer’s disease is a progressive neurodegenerative disorder that impairs memory, cognition, and behavior. It is the most common cause of dementia in elderly individuals and presents a significant public health challenge. The reason why I chose Alzheimer’s disease is because it is an area of research that has gained increasing attention in recent years, with numerous studies investigating its etiology, pathophysiology, and potential treatments. The complexity and multidimensional nature of Alzheimer’s disease make it a compelling topic to explore, as it encompasses various disciplines including neuroscience, genetics, and psychology. Additionally, the impact of Alzheimer’s disease is substantial, not only on individuals suffering from the disease, but also on their families and society as a whole. Understanding the underlying mechanisms of Alzheimer’s disease and developing effective interventions is of critical importance in the field of healthcare. Hence, I believe that working on Alzheimer’s disease would not only provide me with a comprehensive understanding of the disease, but also contribute to the ongoing efforts in combating this debilitating condition.

Alzheimer’s disease was first described by Alois Alzheimer in 1906, and since then, significant advancements have been made in unraveling its intricate pathogenesis. The hallmark neuropathological features of Alzheimer’s disease include the accumulation of amyloid-beta plaques and neurofibrillary tangles composed of hyperphosphorylated tau protein in the brains of affected individuals. These pathological changes lead to synaptic dysfunction, neuronal loss, and ultimately, cognitive decline. The exact etiology of Alzheimer’s disease remains unclear, but both genetic and environmental factors are believed to play a role in its development.

Genetically, mutations in genes such as amyloid precursor protein (APP), presenilin-1 (PSEN1), and presenilin-2 (PSEN2) have been identified in rare familial forms of Alzheimer’s disease. These mutations result in an increase in amyloid-beta production or a shift in the ratio of amyloid-beta isoforms, leading to enhanced aggregation and deposition of amyloid-beta plaques. On the other hand, the apolipoprotein E (APOE) gene, specifically the APOE ε4 allele, is the most well-established genetic risk factor for late-onset Alzheimer’s disease. Carriers of the APOE ε4 allele have an increased risk of developing the disease and tend to exhibit an earlier age of onset.

In addition to genetic factors, certain environmental and lifestyle factors have also been implicated in the risk and progression of Alzheimer’s disease. For instance, cardiovascular risk factors such as hypertension, diabetes, and obesity have been associated with an increased risk of developing Alzheimer’s disease. Chronic inflammation and oxidative stress, both of which can be influenced by lifestyle choices, have also been implicated in the pathogenesis of Alzheimer’s disease. Furthermore, there is growing evidence linking cognitive and social engagement, physical activity, and a healthy diet with a reduced risk of developing Alzheimer’s disease.

Despite the advances in understanding the pathophysiology of Alzheimer’s disease, there is currently no cure for the condition. Treatment strategies primarily focus on symptom management and slowing disease progression. Acetylcholinesterase inhibitors, such as donepezil, galantamine, and rivastigmine, are commonly used to improve cognitive function in individuals with mild to moderate Alzheimer’s disease. Another class of medications, N-methyl-D-aspartate (NMDA) receptor antagonists, including memantine, can be prescribed to individuals with moderate to severe Alzheimer’s disease. These medications provide modest improvements in cognitive symptoms but do not halt or reverse disease progression.

Various research efforts are underway to develop disease-modifying therapies for Alzheimer’s disease. These approaches aim to target the underlying mechanisms of the disease, such as amyloid-beta accumulation or tau pathology. For example, anti-amyloid-beta monoclonal antibodies, such as aducanumab, have shown promise in clinical trials by reducing amyloid-beta plaques and slowing cognitive decline in patients with early-stage Alzheimer’s disease. Other innovative approaches, including tau-targeted therapies and inflammation-modulating agents, are also being explored.

In conclusion, Alzheimer’s disease is a complex neurodegenerative disorder that poses significant challenges to healthcare systems worldwide. Its multifactorial etiology, ranging from genetic to environmental factors, necessitates a comprehensive approach to understand the disease. While current treatment options provide only symptomatic relief, ongoing research efforts hold promise for developing disease-modifying therapies. By studying Alzheimer’s disease, I hope to expand my knowledge in this field and contribute to the collective efforts in combating this devastating disease.