Alzheimer's Disease Discussion

Alzheimer's disease (AD) is a disease that affects a person's mind, according to Brill (2005). When people have this disorder, chemical and physical changes in the brain cause them to behave strangely. The individual ultimately dies due to the various changes that occur in their brain, causing the nerve cells in the region to die. The disorder impairs one's judgment and takes away one's memory. Since it regulates such aspects as movement, breathing, voice, and emotions, the brain is an essential operational component of the human body. It also governs the senses of sound, touch, taste, and smell. As a result, when a person loses their ability to perform these functions, they lose their ability to do so. The current medicine for AD includes a huge unmet medical need and symptomatic treatments, which exist to reverse, stop, and slow the development of the disease. This paper will carry out a pathophysiological research on Alzheimer's disease.
Alzheimer's disease and Dementia
This illness is degenerative and leads to dementia. This is a term used to describe the loss of mental ability as well as memory severe enough to influence the daily life of an individual. AD comprises 60 to 80 percent of all dementias, which makes it the most common type of the disease (Lu & Bludau, 2011). Dementia is a group of occurring symptoms and signs that comprise progressive intellectual function deterioration. Dementia is also a condition that impairs various cognitive abilities, including orientation, attention, visuospatial function, decision-making, reasoning, language, and memory. Furthermore, in people with dementia, the cognitive impairments are time and again accompanied by changes in social behaviors, emotional regulations, as well as personality. Ideally, these behavioral and cognitive changes that occur with dementia interfere with relationships, social activities, and work. Furthermore, it impairs the ability of an individual to carry out daily routine activities such as personal care, managing finances, cooking, housekeeping, shopping, and driving. One must be able to perform these essential activities to function independently in society. However, the brain loses its ability to carry out these core competencies when someone has dementia (Lu & Bludau, 2011).
Types of Alzheimer's disease
The Alzheimer's disease occurs in three basic types. The first one is the early-onset AD, which has characteristics such as premature aging, behavior changes, and memory loss. Less than 10 percent of individuals with AD have this type, and it afflicts people younger than 65. Another form is the late-onset AD, which usually transpires after age 65. It accounts for about 90 percent of cases, which makes it the most common form of AD. The last one is the familial AD, which is often inherited. It affects families whereby at least two generations will suffer from the disease. This type of AD accounts for less than one percent of all cases of the disease making it rare (Kelly, 2008).
Alzheimer's disease and the Brain
The Alzheimer's disease disrupts the numerous operations of the mind. It influences both the activity of the neurotransmitters and the impulses as they travel along the neurons. The primary type of cells that the AD destroys is the neurons. In time, the AD causes tissue and nerve loss throughout the brain. In the brain, the areas affected the most by AD include first the ventricles, which get larger due to the disease. The second one is hippocampus, which is a major structure that plays a crucial role in establishing memories. Nonetheless, AD causes it to shrink. Another part is the cerebral cortex. In this context, the memory, planning and thought part of the brain forms clumps and tangled neurons (Kelly, 2008).
Alzheimer's disease and Neurodegeneration
The AD is a chronic progressive neurogenerative illness. The progression of the symptoms is different from each; however, it can roughly be divided into three stages. These include severe, moderate, and mild. The development of symptoms can be attributed to the progressive and sequential loss of synaptic connections neuronal functions as well as the death of neuronal cells in various parts of the brain. In the mild stage, the disease is first marked with the loss of memory. This is because AD first affects the hippocampus, which is the neuron in the region for memory formation. Here, the patients may forget names and words with escalating intensity and get lost even in places that are familiar to them. The cortical regions responsible for reasoning become affected in the moderate stage. As such, the AD patients may begin experiencing confusion and losing their logical thinking. Consequently, they may have difficulties identifying and recognizing family members. Also, they may need assistance putting on appropriate clothing suitable for the season (Lau & Brodney, 2008).
Transformation in personality may as well transpire due to AD. For instance, there may be inappropriate screaming and kicking, as well as, cursing and making an accusation of fidelity and theft. Additional brain regions are damaged in the severe stage. This causes loss of responses to the external environment and loss of control of numerous physiological functions. The AD patients lose their ability to speak coherently as well as their capacity to take care of their daily living. This means that they will require assistance with walking, toilet use, and feeding. The deterioration of the brain’s control of critical physiological operations is the principal cause of death of patients with AD. This is because it results in deadly complications, including a real fall, urinary tract infection, or pneumonia (Lau & Brodney, 2008).
Pathological features of Alzheimer's disease
Microgliosis
Clusters of reactive microglia surround the amyloid plaques in AD brains. This phenomenon is referred to as microgliosis. The activation of microglia impairs the cognitive functions and leads to activated renal cells. Nonetheless, engagement in social, mental, and physical activities has been shown to trim down the risk of developing AD (Lau & Brodney, 2008).
Tau Pathologies
In AD, the tau pathologies play a considerable role in the deterioration of the neuronal health. The correlation with clinical manifestation and neurodegeneration, as well as, the subsequent evolution of tau pathologies suggest that although tau pathologies are not the ultimate trigger of AD, they play a prominent role in the demise of neurons. The tau pathologies may cause neurodegeneration in two ways. These include the gain of toxic functions and the loss of essential services. For this reason, the reduction of tau toxicities, as well as tau pathologies, is a crucial area in the fight against AD (Lau & Brodney, 2008).
Amyloid Pathologies
Although not a unique characteristic feature of AD, neurodegeneration is a crucial trait in the disease. The presence of the telltale pathologies in the brains of the patients is what distinguishes AD from other neurodegenerative diseases. The revealing pathologies include the neurofibrillary tangles and amyloid plaques. The Aβ is what sets off a whole cascade of events. This involves the generation of NFTs, which ultimately causes loss of brain function and neurodegeneration in AD patients. Furthermore, it has been shown that the Aβ peptides damage the hippocampal long term potentiation (LTP). The LTP is a cellular process that is perceived to be the source of memory as well as learning in vivo and vitro (Lau & Brodney, 2008).
Diagnosis of Alzheimer's disease
The standard for the AD diagnosis is an autopsy-based pathological assessment. The distribution and the presence of the NFT and amyloid plaques in the brain are applied to stage the disease and to ascertain the diagnosis of the definitive AD. The diagnosis of AD in the clinical setting is primarily based on the neuropsychological evaluation, physical and neurological examinations, and medical history, as well as the exclusion of various etiologies by applying selective ancillary testing. The accuracy of the diagnosis of AD in the clinical setting is 70 to 90 percent compared to the pathological diagnosis. On this note, greater efficiencies are attained in the area of expertise such as memory disorder clinics. When the cognitive impairment of the patient is suspected to be as a result of other etiologies or has an atypical clinical course besides AD, the physicians recommend a possible AD dementia. The patients with AD often have normal findings on neurological as well as physical examination. Moreover, the non-contrast computed tomography (CT) or the structural magnetic resonance imaging (MRI) may be useful in the diagnosis of AD. This is because they may be helpful in ruling out common cerebrovascular lesions, brain tumors, cerebral hematomas, and pressure hydrocephalus (Korolev, 2014).
Treatment of Alzheimer's disease
The AD has no cure, and the drug therapy for the illness is still in the early stages. When it comes to treating the disease, the approved medications does not reverse the course of the illness itself or slow it down, but it controls the symptoms. Currently, the mainstay of the AD therapy is drugs intended for neurotransmitter system in the brain. The Acetylcholinesterase inhibitors assist in enhancing attention as well as memory function in AD patients. The inhibitors achieve this by hampering the acetylcholine breakdown, which, in turn, boosts the neurotransmitter levels at the synapse. At present, there are three approved cholinesterase inhibitors for FDA. These include first donepezil for all AD stages and secondly galantamine and rivastigmine for mild to moderate AD (Korolev, 2014). Additionally, the knowledge on AD has produced some possible therapeutic strategies for the illness. Some of the approaches are believed to be disease modifying while others are symptomatic. The modifying ones are considered to be able to reverse, halt, or slow the progression of the AD. The approach to treat AD aims either at compensating for the operational deficit or ameliorating the pathologies to restore normal functions (Lau & Brodney, 2008).
Conclusion
The AD is an illness that is complicated, and it is imminent in the aging population, which increasingly exposes them to various risk factors. Nonetheless, the improved knowledge of the disease, as well as its pathologies, has created a myriad of rational therapeutic strategies. Some of these are being tested in preclinical studies while others are being investigated in clinical trials. Both diseases modifying and symptomatic strategies will be crucial in promoting the overall well being of AD patients. Increasing resistance by engaging in social, mental, and physical activities, as well as, reducing risk factors such as obesity, diabetes, and hypertension may ward off the possibility of contracting AD. The disease is a rapidly, multifactorial, and complex neurodegenerative disorder portrayed by progressive dementia and cognitive impairment (Shakeri, 2017).
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References
Brill, M. T. (2005). Alzheimers Disease. New York: Benchmark Books.
Kelly, E. B. (2008). Alzheimers Disease. New York: Chelsea House.
Korolev, I. O. (2014). Alzheimer’s Disease: A clinical and basic science review. Medical Student Research Journal, 4, 24-33.
Lau, L., & Brodney, M. A. (2008). Alzheimers Disease. Berlin, Heidelberg: Springer-Verlag Berlin Heidelberg.
Lu, L. C., & Bludau, J. (2011). Alzheimers Disease. Santa Barbara, CA: Greenwood.
Shakeri, A. (2017). Design, Synthesis and Biological Evaluation of Novel Adamantane Derivatives as Potential Treatments for Alzheimer’s Disease (Master's thesis, University of Waterloo).