Synapse and Dysfunction in Alzheimer Essay

Introduction

Alzheimer disease is said to be predominantly caused by amyloid peptide as the cascade that is the most significant contributor to the disease. Dysfunction is reported to be generated by soluble assembly of states of amyloid peptide. Alzheimer is also said to be a progressive mental deterioration which tends to occur in the middle of old age due to the process by which the brain generally faces degeneration. Dementia is the main problem caused by Alzheimer disease since Alzheimer is connected to the loss of an individual's cognitive functioning and their behavioral capabilities thus a person's daily activities and life processes are challenged. Kvartsberg et al. (2015) outlined that dementia as a result of Alzheimer develops in intensity from mildest stage to a more advanced stage (Kvartsberg et al., 2015). Mild dementia is recorded when a person's functioning starts to be challenged and becomes severe when the person tends to develop dependability even in more essential things in life. Early onset of Alzheimer is associated with genetic mutation, and later it appears to be a series of cognitive changes. This paper seeks to analyze Alzheimer as a disease and the conditions that make Alzheimer to be diagnosed by focusing on synapse and dysfunction occurrences.

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Synaptic Loss and Dysfunction as the Indicator of Alzheimer

Synapse and dysfunction happen in the brain leading to dementia which is a cognitive dysfunction which tends to affect the normal behavioral abilities thus affecting a person's daily and regular functions. Synaptic dysfunction is considered in the diagnosis of Alzheimer when several amyloid peptides (Av) are recorded in several oligomers targets and various cellular mechanisms which are responsible for Av-induced synaptic failure (Lee et al., 2018). Therefore, when an Av-induced synaptic complication and failure have been identified, synapse and dysfunction in Alzheimer are considered. Additionally, whenever an individual record weird physiological roles, synapse, and dysfunction are supposed to be conditions to determine the prevalence of Alzheimer. Loss or normal function is said to be caused by amyloid peptide (Av) thus synapse and dysfunction is considered a test for Alzheimer disease.

When the patient records neuronal and synaptic losses in conjunction with degeneration and alteration of composition and structure of the membrane, viable targets are provided whenever synapse loss and membrane-related pathology tend to offer workable targets that are relevant in the intervention of Alzheimer disease (Peters-Founshtein et al., 2018). Whenever the patient's urine depicts to comprise of uridine, docosahexaenoic acid, choline, folic acid, vitamin B12, B6, C, and selenium, then the patient is considered to be eligible for the measure of synapse losses and dysfunction in line with Alzheimer disease.

When a patient portrays memory dysfunction, then the patient is then subjected to the diagnosis of Alzheimer disease. It requires keen study of the patient's past ways of doing things as a way of determining their level of memory and to decide whether or not they face memory dysfunction as an indication of the prevalence of Alzheimer disease (Peters-Founshtein et al., 2018). The most aspects that make synapse loss and dysfunction to be indicators of incidence of Alzheimer is the changes in personality, disorientation, short-term and long-term memory loss.

Why it is Still Not Possible to Interfere with Alzheimer's Progression and Cure

Alzheimer's disease is said to be a mental progression and deterioration that takes place in stages without the patient knowing the changes in their psychological well-being. Additionally, Alzheimer causes dementia as a result of some form of generalized degeneration of the patient's brain (Peters-Founshtein et al., 2018). A person's changes in daily life and mental functioning cannot be detected during their early stages since humans are not subjected to an intensive track of their mental capabilities and changes in their general wellbeing. The other issue is that scientists have not yet determined the cause of Alzheimer disease. Even though it has been identified that genetic mutation of some patients results in Alzheimer disease, the exact time that the problem starts has not been defined. The series of brain changes are inconsistent thus it is difficult for practitioners to determine the specific changes in the patients' cognitive ability. Combination of genetic changes in the patients makes it difficult for the progression and cure of Alzheimer to be practically achievable (Lang & Fowers, 2018). Environment and an individual's lifestyle should be taken into practice as a way of determining their mental changes in conjunction with Alzheimer disease.

The factors associated with Alzheimer are diverse and not proven thus it is difficult to predict the outcome of treatment and possible preventive approaches for Alzheimer disease (Lang & Fowers, 2018). Mental dysfunction and synaptic loss are not easily noted in an individual thus it is quite difficult to achieve the required treatment for patients with Alzheimer disease. Additionally, Alzheimer disease tends to affect an individual at their old age and mostly in their mid-60's where people's behavior usually changes as a result of aging. Synaptic loss and dysfunction become difficult in determining the cause of Alzheimer in conjunction with possible treatment of the disease. Apolipoprotein E gene is said to be involved in the onset of Alzheimer experience, and it is said to take many forms. Also, APOE E4 is said to be one of the genes forms that tend to increase an individual's risk of developing Alzheimer at an early age or onset of the disease. Therefore, it has been found out that carrying out APOE E4 gene does not necessarily mean that an individual will tend to develop Alzheimer disease (Lang & Fowers, 2018). The fact that people who don't even have APOE E4 gene have been reported to create the disease shows that it is difficult to find a perfect treatment for Alzheimer disease.

In 2014, people of all ages were found to have Alzheimer disease thus portraying many challenges to the possible way of treating and managing Alzheimer's disease and the associated synaptic loss and dysfunction. Since Alzheimer affects the three processes that tend to keep neurons healthy, i.e., communication, repair and metabolism, it is not easy to detect that metabolic problems imply the onset of Alzheimer disease. In synaptic loses, some nerve cells in an individual's brain tend to stop working thus losing connection with the other nerve cells in the brain thus leading to the death of the nerves (Lang & Fowers, 2018). Memory loss results after the death and destruction of specific nerve cells that tend to be excommunicated from other brain cells. Senile plaques tend to build up thus resulting in the onset of Alzheimer thus leading to the loss of neurofibrillary tangles which affect cognitive abilities.

Chemical characterization of amyloid protein and the possible sequencing of the chain of amino acid are not well studied regarding their characteristics. Cloning and encoding of the precursor protein result into various challenges towards finding the solution and preventive measures towards Alzheimer disease. The loss of cognitive abilities is accompanied by multiple difficulties of life thus not suitable to determine the cause of Alzheimer and possible ways of controlling the effect (Zhang, Li, Feng, & Wu, 2016). There are recent discussions concerning the occurrences of various challenges associated with problematic mental issues that are not easily detected. Cloning of gene results into multiple precursors related to protein precursors thus there is no chance for providing an array of scientific information concerning the ways of treating and managing Alzheimer disease and possible precursors associated with the disease (Zhang et al., 2016). Amyloid deposition in the brain is among the challenges that tend to affect the mechanism towards controlling Alzheimer disease.

Identification of the fact that a person has Alzheimer is easy to tell by the approaches of physicians but not easy to determine the cause of dementia. Also, diagnosis of Alzheimer complications requires a set of criteria after careful medical evaluation and mental status testing. Additionally, there is the need for the physical, neurological exam, brain scan, and blood tests. Prognosis of the patients with dementia has been a significant problem since the onset of the disease is not easily detected in normal circumstances (Zhang et al., 2016). Additionally, the process of identifying Alzheimer disease is usually after various brain cells and nerves have been destroyed due to lack of proper communication within the brain cells. Therefore, the progression of cure of Alzheimer disease is not quickly done because a significant number of cells are usually destroyed at the realization of the condition in a patient.

There is no proven new treatment for Alzheimer disease thus asserting that following treatment of Alzheimer is not confirmed (Zhang et al., 2016). There are several treatment approaches towards saving an individual who portrays to have Alzheimer in their usual mental strategies, but the medication upon them fails to protect them from the impending danger that results from severe dementia, synaptic loss, and dysfunction. Kamat et al. (2016) mentioned that old age guarantees the quick death of the patients diagnosed with Alzheimer thus showing that there are no explicit medical or preventive approaches that have been identified about Alzheimer and its effect on people. Identification of memory loss and behavioral changes tend to happen late thus treatment of Alzheimer becomes difficult.

Kamat et al. (2016) outlined that the interneuron connections get damaged thus resulting into the stoppage of the permission of neuronal passage of electrical and chemical signals to all possible cells which is a fundamental process in the whole body functioning of a rational human being. The damage to the neurons is said to be irreversible thus confirming that synaptic loss and synaptic dysfunction is a condition that affirms that the patient of Alzheimer cannot be well treated from the impending dangers of the complication just after it has been detected. The synapsis dysfunction and the synaptic loss is the reason for cognitive deficits that are typically recorded in a patient.

When Synaptic Losses and Dysfunction is Considered

Neuronal dysfunction as induced by Av offers a chance for the analysis of a patient to be having Alzheimer disorder. The progression of the disease is taken to be determined through the establishment of the elevated levels of Av oligomers which are said to disrupt the normal functioning of the body synaptic processes including the synaptic plasticity thus triggering memory loss and various cognitive deficits. The inoculation of Alzheimer disorder transgenic in conjunction with Av or conceivable against Av antibodies tend to lessen amyloid plaque prevalence (Koffie et al., 2011). The process of clearing existing plaques and the issues that result in the formation of Alzheimer disorder comes about into subjective shortages in this manner proposing that the evacuation of Av as a change is fundamental to the mind.

When the practitioners find out that Av in oligomeric shapes is dangerous to neural connections, they consider it to be a viable sign for the synaptic damage and loss. Therefore, the factor confirms that it is a practical time for reviewing the diagnosis of the patient for the presence of Alzheimer disease. Thus, the condition leads to the need for counteractive action against Alzheimer disease (Koffie et al., 2011). Most Av items have been...