Alzheimers Disease Symptoms, Stages, Causes and Treatments - Free Essay Example

Sample details Pages: 7 Words: 2025 Downloads: 10 Date added: 2019/04/12 Category Medicine Essay Level High school Tags: Alzheimer's Disease Essay Did you like this example? Introduction The brain is a significant and complex organ with a vast array of roles necessary for sustaining human life. Some of these include cognitive functions, homeostatic regulatory responsibilities, motor controls, and sensory information reception. While the human brain has numerous capabilities essential to life, a wide range of neurological disorders can impede these, causing a variety of potentially fatal diseases, such as Alzheimers disease. German physician Dr. Alois Alzheimer first described Alzheimers disease as presenile dementia in 1906. Now known to be a progressive neurodegenerative disorder, Alzheimers disease is the most common form of dementia, accounting for nearly 35 million cases globally (Martorelli, et al.). In the United States today, it is speculated that someone develops Alzheimers disease every 66 seconds, however in 2050, a new case of Alzheimers is expected to develop in as little as every 33 seconds (Alzheimers Association). Subsequently, since Alzheimers disease has become much more widespread, it has also become much more fatal. As of 2014, in the United States alone, the disease was reportedly responsible for approximately 85,000 deaths. Moreover, during the years 2000 to 2013, the number of deaths caused by Alzheimers disease increased by over 71%, while mortality caused by stroke, heart disease, and prostate cancer actually decreased by 23%, 14%, and 11%, respectively (Alzheimers Association). However, it is important to suggest that these mortality statistics may be greatly underestimated since death certificates may list other complications as causes of death, rather than the underlying Alzheimers disease. Don’t waste time! Our writers will create an original "Alzheimers Disease: Symptoms, Stages, Causes and Treatments" essay for you Create order Additionally, a key aspect of the surging prevalence of Alzheimers disease as a fatal disorder is that it is only intensifying with increasing longevity in humans. For example, in his article Pathogenesis of Alzheimers disease, Dr. Russell Swerdlow, the Director of the University of Kansas Alzheimers Disease Center and the KUMC Neurodegenerative Disorders Program, references a survey of brains from persons over the age of 85 that all showed evidence having at least some degree of Alzheimers disease. He states that therefore, it is worth considering that at some point in the aging continuum, Alzheimers disease ceases to become a disease because it becomes a norm. Thus, as the facts and statistics stated above may imply, Alzheimers disease is becoming a widespread disease characterized as much more than the memory loss commonly associated with it. Unfortunately, however, the diagnosis of Alzheimers disease is primarily reliant on observations of cognitive and functional decline (Martorelli, et al.). These symptoms include: agnosia, the loss of perceptual ability regarding the interpretation of sensory perceptions; apraxia, the inability to understand the meaning or appropriate use of things; and dysphasia, the failure to arrange words in a meaningful manner (Martone and Piotrowski). Therefore, due to the complexity and extent of the neurological deficits that which it causes, Alzheimers disease is typically terminal once it has finally been diagnosed. In addition to its inability to be diagnosed through practical medical testing, Alzheimers disease is even more so fatal as a result of the uncertainty behind its physiological causes and the lac k of a known cure. Causes An early feature of Alzheimers disease is synaptic loss that renders neurons dysfunctional and prone to irreversible death, ultimately precipitating the severe brain atrophy and cognitive impairment observed in later stages of the disease (Seddighi, et al.). Simply put, Alzheimers disease causes the volume of the brain the shrink considerably. However, there are several hypotheses as to why this happens. The most well-known theory, the amyloid cascade hypothesis, has been the mainstream concept underlying Alzheimers disease research for more than 20 years (Kametani and Hasegawa). Usually resulting from genetic mutations on chromosome 21, this hypothesis states that various pathological changes occur in response to abnormally increased concentrations of beta-amyloid protein (Widmaier, et al). This protein is derived from its much larger precursor, the beta-amyloid precursor protein (APP), by two proteases, beta-secretase and gamma-secretase. Specifically, a mutation in two amino acids (lysine and methionine mutated to asparagine and leucine) of APP adjacent to the beta-secretase site is known to increase beta-secretase activity and thus, beta-amyloid protein production (Martone and Piotrowski). In addition to mutations affecting chromosome 21, the specific mutations of the genes presenilin 1 and presenilin 2 associated with chromosomes 14 and 1, respectively, also result in the increased production of the beta-amyloid protein. Alternatively, this protein is the much larger and more pathogenic version, which is known as the beta-amyloid protein 42 (Martone and Piotrowski). Because of this, the two presenilin mutations usually trigger an early onset of Alzheimers disease, and presenilin 1, specifically, can even occur in patients as early as age 30. Therefore, it can be inferred that Alzheimers disease caused by mutation of the presenilin 1 gene is characterized as being far more malignant than the other forms of the disease. Not only is this due to its extraordinarily early onset, but it also is the result of its increased aggression characterized by the abundance of amyloid plaques in more detrimental regions of the brain, such as the cerebellum (Martone and Piotrowski). As stated previously, the increase in beta-amyloid protein production results in a triad of of pathological changes, including the formations of senile plaques, amyloid angiopathy, and neurofibrillary tangles. To elaborate, senile plaques consist of amyloid deposits surrounded by dystrophic neurons, while amyloid angiopathy is the presence of the same deposits within the brain vasculature. Neurofibrillary tangles, on the other hand, are simply tangled fibrillary protein aggregates within nerve cells of the brain, but, however, these components have drawn quite a bit of attention lately (Martone and Piotrowski). Some scientists have begun to develop a new hypothesis focusing on the neurofibrillary tangles as the basis of their Alzheimers research. Neurofibrillary tangles specifically contain abnormally configured and excessively phosphorylated tau protein. This is significant because in most differentiated cells, tau is generally unphosphorylated and is responsible for associating with microtubules to form a permanent cytoskeleton (Swerdlow). The human tau gene is localized on chromosome 17, and as the result of mRNA alternative splicing, it has six known isoforms expressed in the adult human brain. In other neurodegenerative disorders, such as frontotemporal dementia, mutations associated with the tau gene result in either protein accumulation, which causes neuronal degeneration, or impairment of microtubule regulation, ultimately leading to extensive cell damage (Kametani and Hasegawa). Furthermore, recent positron emission tomography (PET) studies have shown that the spatial patterns of t au tracer binding are closely linked to the patterns of neurodegeneration and clinical presentation in Alzheimers disease patients (Kametani and Hasegawa). In addition, tau lesions in the brain have also been shown to occur earlier than beta-amyloid protein deposits. Therefore, it is believed that Alzheimers disease progression is more reliant on tau pathology than amplified beta-amyloid protein production (Kametani and Hasegawa). Somewhat humorously, there has been a long-standing debate regarding the significance of the pathological findings in Alzheimers disease. This argument has questioned whether beta-amyloid-protein-associated pathology or the tau-protein-associated pathology is the primary lesion in the disease, which therefore has divided investigators into baptist and aoist camps (Martone and Piotrowski). For example, on one hand, some may argue that the amyloid plaques are a result neurodegenerative processes, such as normal aging or neurofibrillary tangle-associated neuronal degeneration, rather than their cause. On the other hand, however, others may argue that there have been no direct links between the genetics of Alzheimers disease and the tau protein, even though a mutation has been identified in tau when its associated with non-Alzheimers dementia, or frontotemporal dementia (Martone and Piotrowski). Nevertheless, outside of this debate an additional theory, the mitochondrial cascade hypothesis, has recently arose. This idea assumes that similar physiological mechanisms underlie both Alzheimers disease and common brain aging. More importantly, it postulates that since Alzheimers disease mitochondrial dysfunction is systemic, it cannot be a consequence of neurodegeneration (Swerdlow). In contrast to the amyloid cascade hypothesis, which is based on studies of rare, autosomal-dominant mutants, this proposal looks to determine the causes of common late-onset, sporadic Alzheimers disease. In this model, the makeup of an individuals electron-transport chain is inherited and gene-specific. The chain sets basal rates of reactive oxygen species (ROS) production, which therefore determines the rate at which mitochondrial damage occurs. As a result, oxidative mitochondrial DNA, RNA, lipid, and protein damage amplifies ROS production and triggers three events (Swerdlow and Khan). First, it signals a reset response in which cells respond to the elevated ROS by generating the beta-amyloid protein, which further impedes mitochondrial function. Then, it prompts a removal response in which compromised cells are disposed of through apoptosis mechanism, and finally, it generates a replace response in which neuronal progenitors unsuccessfully attempt to re-enter the cell cycle, which results in aneuploidy, tau phosphorylation, and neurofibrillary tangle formation (Swerdlow and Khan). Ultimately, the probable causes of Alzheimers disease all converge at one main idea: Alzheimers disease is the direct result of neuronal degeneration and decreased synaptic density due to some sort of protein accumulation within the tissues of the brain. Therefore, due to neuronal death, there is a widespread decline in various neurotransmitter-containing cell bodies of the brain. However, the most consistent losses throughout the progression Alzheimers disease are that of the cholinergic neurons of the basal forebrain (Mufson, et al). Despite this congruence, however, understanding the pathophysiological mechanisms that drive neurodegeneration, and therefore the subsequent acetylcholine deficits, in Alzheimers disease is crucial for rationally designing neuroprotective agents capable of preventing the disease progression (Coimbra, et al.). Treatments Currently, the treatment options available for patients with Alzheimers disease are primarily palliative options that only address and temporarily alleviate symptoms of the disease. Some of the most common treatment options include acetylcholinesterase inhibitors, such as donepezil, rivastigmine, galantamine, and tacrine, to name a few (Martone and Piotrowski). By inhibiting acetylcholinesterase, these agents therefore inhibit the degradation of the neurotransmitter acetylcholine, which is commonly reduced in individuals with Alzheimers disease due to neuronal degeneration (Widmaier, et al.). In addition, nonsteroidal anti-inflammatory drugs (NSAIDs), such as aspirin and ibuprofen, are also commonly prescribed in order to limit any inflammatory responses in the brain that may have been caused by any neurotoxic effects of the accumulation of the beta-amyloid protein (Martone and Piotrowski). Furthermore, because of the limited effects of pharmacological treatments, the use of psychological and psychosocial interventions has become increasingly popular in recent years. This method, known as cognition-focused intervention is commonly partitioned into three separate approaches: cognitive stimulation (CS), cognitive training (CT), and cognitive rehabilitation (CR). In short, CS aims to enhance cognitive function through participation in a set of activities that engage mental processes, CT aims to improve specific cognitive functions through a set of standardized tasks with guided practice, and CR aims to address the impact of cognitive impairment of everyday functional ability in order to reduce disability and improve functioning in specific activities of daily living (Oltra-Cucarella). More importantly, in order to better the lives of those afflicted and to decrease the overall mortality rate caused by Alzheimers disease, research on new possible treatments is underway. For example, several groups of researchers worldwide are actively attempting to discover and develop beta-secretase inhibitors in order to limit the proteolytic processing of APP that subsequently produces beta-amyloid protein (Coimbra). Thus, by inhibiting the accumulation of this protein, these potential cures could stop the progression of Alzheimers disease in its tracks. As a result, not only would this hypothetical cure improve the quality of life for those afflicted with Alzheimers disease, but it would also increase the chance of prolonged survival. Conclusion Although Alzheimers disease was first characterized in 1906, we, as humans, still have much to learn about the neurodegenerative disorder, even over 110 years later. Despite having a plethora of possible genetic causes, this disorder is generally classified as a progressive neurodegenerative disease. On the surface, Alzheimers disease seems as though it is simply portrayed as memory loss due to a net shrinkage in brain volume. However, this is far from the truth. Alzheimers disease is characterized by neurological degeneration and degradation caused by protein accumulation, whether it be beta-amyloid plaques or tau protein. As a result, this disease is associated with a variety of cognitive deficits, including agnosia, apraxia, and dysphasia, and it typically results in fatality. In summary, Alzheimers disease research is incredibly significant to the lives of over 30 million people affected worldwide, making it one of the leading causes of death across the globe.