Alzheimer's disease is an insistent disorder that leads to the deterioration and wastage of brain cells. One of the most known causes of Alzheimer's disease is dementia. Dementia is a state of continuous decline in social skills, behavioral skills, and thinking. Dementia interrupts the ability of an individual to function independently. An individual with Alzheimer's disease keeps forgetting recent conversations and events. This is an early sign of the disease. Severe memory impairment could be experienced as the disease progresses, and patients could lose their ability to carry out simple day-to-day tasks.
The current medication and treatment of Alzheimer's disease mostly suppresses its progress and slows down the decline rate. The treatment is mostly a temporary solution to improve its symptoms. Alzheimer's disease patients could rely on these treatments to continue carrying out their day-to-day functions and maximize being independent for a while. Caregivers have developed different programs that could help patients live with Alzheimer's disease. There still is no cure that heals Alzheimer's disease what suppresses its activity in the brain. Patients develop other signs and symptoms in advanced stages of the same disease. These symptoms may include malnutrition, dehydration, and the patient could die of infections. The study will conduct the pathological changes that result from the contracting of Alzheimer's disease. Some of the pathological changes covered within the study include neuronal death, the development of neurofibrillary tangles, the presence of amyloid plaques, and glial hypertrophy.
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The study will further investigate the disruption of myelin in Alzheimer's disease patients. The destruction of myelin in Alzheimer's patients was first discovered in 1911 by Alois Alzheimer. Most scientists have, however, not put much attention on developing this study. Most of the observations made by Alois Alzheimer have escaped the attention of most modern researchers. This study will dig in to find evidence of myelin pathology in Alzheimer's patients.
Goals and Objectives
This study aims to determine if myelin impairment is the first sign and symptom of Alzheimer's disease. The research will also investigate the defection caused by the disease on the biosynthesis of mile and lipids. This is mostly experienced in the preclinical stage. Another objective of this study will also include investigating the contributors to the significant deterioration of synaptic function and the factors that lead to cognitive decline in Alzheimer's disease patients. Based on prior studies, cognitive decline and synaptic dysfunction mostly cost over time and persistent myelin damage. The study will also aim to investigate the allegations published by some researchers that indicated that myelination is the first step to developing Alzheimer's disease. These studies argued that Alzheimer's disease could only develop after myelination has occurred.
This study will first investigate the role mining plays in Alzheimer's disease and analyze the data based on animal models. The study will also dig to find further proof of myelin’s role in cognition. The explanation and discussion will be done on the myelin damage in Alzheimer's disease. The final objective of this research will be to examine the causes of myelin damage in Alzheimer's disease.
Methodology
The study obtains its data from published secondary materials. The study relies on previous works on Alzheimer's disease and develops general knowledge of most researchers' perspectives. However, most research ignored the critical role that myelin disruption plays in the advancement of Alzheimer's disease. The evidence of myelin pathology based on data provided from prior studies will be considered. All research was conducted and published since Alzheimer's disease is considered relevant for the study. Most of the arguments presented in this study are developed from the first published research on Alzheimer's disease in 1911 by Alois Alzheimer. Over 100 years of compiled and published research have, therefore, been considered for this presentation.
Results
This study aimed to investigate the evidence that myelin deficiency plays an essential function in developing Alzheimer's disease. Several aspects of myelin impairment investigated include myelin's role in the advancement of Alzheimer's disease, the role of myelin in cognition, the damaging of myelin in Alzheimer's disease, and the cause of myelin damage in Alzheimer's disease. All the results of the study have been presented below and discussed below.
Data on The Function of Myelin from Animal Models
The action potentials on the nerves are generated at the nodes of Ranvier. The nodes of ranvier and the axons provide a surface that myelin wraps around. The number of ranvier nodes and the myelinated axons determine the conduction velocity of the action potentials. Previous studies conducted showed evidence of a decline in synaptic staining and impaired synaptic transmissions in the myelinated axons. The study also found out that the plaques in the neocortex also exhibited focal demyelination.
The Role of Myelin in Cognition
Mylan develops from childhood right through adolescents to adulthood. Various parts of the brain and the central nervous system are myelinated at different times. The study data shows that myelination of the corpus callosum did not occur until the age of 30. The frontal lobes remain unmyelinated until the age of 40. Older people can increase. They are white matter through memory training, which also results in improved cognitive capacity. Therefore, it is evident that mile in damage in older people promotes to the continuous cognitive decrease in strong aging persons.
Myelin Damage In AD
Weak association between the amyloid plaque lesion load and the indications of Alzheimer's disease is low. The study also discovered a weak association between the amyloid burden of Alzheimer's disease patients' brains and brain atrophy intensity. The studies reviewed by this study shows that human brains of Alzheimer's disease patients had fewer oligodendrocytes. The study also discovered that the initial stages of Alzheimer's disease also decreased myelin-associated proteins and the mile in lipids.
The Cause of Myelin Damage In AD
The rate of myelin damage increases with age, and this applies to Alzheimer's disease patients too. The research discovered that the volume of white matter decreases by 28% from adolescence to adulthood, while the volume of liquid enterocytes decreases by 27% from adolescence to adulthood. Delivery from the brain is hindered by reducing the illegal dendrocytes that come smaller in Alzheimer's disease patients. This is because of the degeneration of oligodendrocyte progenitor cells that oligodendrocytes generate. Myelin damage could also occur from the inflammatory process caused by Alzheimer's disease. The release of inflammatory cytokines on the activation of microglial reduces toxins removal's effectiveness from the brain.
Discussion
Axons get sheathed by myelin to the age of 50. As one ages, the mining becomes more susceptible to damage. At this old age, the ineffective ability of myelin to fully perform its functions leads to the build-up of toxic amyloid-beta fibrils. The deposit of toxic amyloid-beta fibrils in the brain and leads to the development of plaques which have long been linked to Alzheimer's disease. The continued cell destruction by the deposited toxic amyloid-beta fibrils distracts the brain signaling. This leads to death cells and the development of symptoms of the Alzheimer's disease.
An example of demyelinating disorders that could be used to compare myelin damage between patients is multiple sclerosis. Impaired cognition is one of the resulting symptoms of multiple sclerosis disease. The data discovered by the study insinuated that 43 to 70% of multiple sclerosis disease suffer from impaired cognition. 64 to 67% of multiple sclerosis disease patience show evidence of myelin damage. Therefore, the data presented makes it more apparent that myelin damage directly affects the diminishment of cognition. The study strongly correlates myelin and the pathology of oligodendrocytes instead of the initial Alzheimer's disease pathology that linked neural degeneration to the reduction in patient's cognition.
Myelin and oligodendrocytes are some of the most iron containing within the brain. Age-related neurodegenerative diseases like Alzheimer's could be because of insufficient iron supply to the brain. The development of amyloid oligomers and plaques comes from the released iron during the breakdown of the late-myelinating regions.
Conclusion
This study aimed to determine if myelin impairment is the first sign and symptom of Alzheimer's disease. The research also investigated the defection caused by the disease on the biosynthesis of mile and lipids. This is mostly experienced in the preclinical stage. Another objective of the study was to include the investigation of the contributors to the significant deterioration of synaptic function and the factors that lead to cognitive decline in Alzheimer's disease patients. Scientists have revealed more evidence on the correlation between myelin and the cognitive reduction in Alzheimer's disease patients. Data from the most recent studies show that other diseases that result in demyelination have reduced patients' cognitive ability as a symptom. Cognitive decline and the degenerative neuro process can be considered to a greater extent as phenomenon caused by demyelination. The study concludes that myelin performs a more significant role in Alzheimer's disease pathology than most of the prior studies have presented. However, myelin and Alzheimer's disease pathology's fundamental role should be further investigated through biochemical, neuropathy analytical, and radiological studies.
