April 28, 2017 at 2:03 am #18394matthewparton91Participant
Hello fellow seekers of knowledge. I am currently writing an essay on Alzheimer’s and the differences in the brains between a healthy individual and a person suffering from the disease. i have fallen behind on the overall assignment and am currently focusing on a ”visual learning aid” on the fight or flight response. i was wandering if i could get an opinion on my essay so far. i will be getting marked for academic writing which is not my strong point. any advice would be greatly appreciated. i have also structured a timeline of the Reisberg scale with an annotated diagram of the brain showing which parts are effected at each stage, which is also not quite finished…..my goodness!! will i ever learn! I always seem to manage a justification for my procrastination!
I cant seem to attach the document so ill copy it onto here if that’s OK, hope its bearable:P!
Alzheimer’s disease (AD) is a neuro-degenerative disease that effects an estimated 44 million people worldwide each year, and around 800,000 people in the UK alone. It is the most common cause of senile dementia, which for centuries has been seen as a normal part of aging, in fact it is not. The average life expectancy after diagnosis is 10 years, but can range from 3-20 years. This depends on the patients age, stage of diagnosis, and lifestyle. Symptoms may appear at 50-60 years of age or later, although occasionally affecting younger individuals.
Later onset of AD has been traced to a gene on chromosome 19 that codes for proteins involved in cholesterol transport. The early onset of AD has been linked to genes on chromosome 21 and 14. People with down syndrome carry an extra copy of chromosome 21 and are at increased risk of developing early onset of AD. Within the information in chromosome 21 are the instructions to produce a protein called amyloid precursor protein (APP), which will be discussed further in this essay. It is thought that a mixture of genetics and environmental risk factors increase the chance of Alzheimer’s.
AD was first discovered by the German scientist Dr. Alois Alzheimer in 1910. A woman named Auguste. D arrived at his clinic who claimed she could not remember who she was. After her death, Dr. Alzheimer dissected the woman’s brain and found there was a significant reduction in size, along with the presence of what we refer to as ‘plaques’ and ‘tangles’.
Amyloid precursor protein is present on the cell membranes of our neurons and many other cells in our bodies. The main purpose of this protein isn’t fully understood but it is involved in synapse formation, neuron plasticity, neural growth and repair, and iron transport. This protein is split into multiple pieces by the enzyme ‘Beta secretase 1’. This protein can often malfunction and cause multiple problems. It is associated with around 20 different disease’s. One of the segments of APP is called ‘beta amyloid’, whose main function is not fully understood but one function that has been discovered is assistance in the regulation of cholesterol transport. It is very sticky and sometimes if it is not regulated correctly, these beta amyloid fragments stick to each other, along with other organic materials, forming what is referred to as a ‘plaque’ on the dendrites of the neuron. These plaques hinder the neurons ability to receive communication from other neurons around it. It was previously though that the production of too much Beta amyloid was the cause for the build-up of plaques, but new studies show that it is a persons’ ability to degrade the protein (Staff, 2010).
Within a nerve cell, there is a highway of microtubules which transport nutrients to the neuron and give the cells axon a stable structure. Helping to support the structure of the microtubules is a protein called ‘Tau’. Tau allows nutrients to pass through freely. In AD, Tau protein changes its shape, this causes the microtubules to collapse which bind with the Tau to create a “Neurofibrillary tangle”. The build of these tangles block the neurons vital supply of energy and nutrients, also hindering communication with other neurons around it. Amyloid Plaques can be present in the brains of healthy individuals, but it is only in the brains of patients suffering from Alzheimer’s disease, where the build up of neurofibrillary tangles are recognised.
The build-up of these plaques and tangles causes the body to see the neuron as faulty, activating the process of apoptosis ultimately destroying the cell. Nerve cell death and tissue loss leads to significant reduction in size of the brain. This effects nearly all functions of the brain. Recent studies suggest that faulty Tau protein can be released into the ECF by an active process of secretion, and taken on by other neurons through endocytosis. Faulty Tau propagates and spreads through the brain in a very predictable pattern during Alzheimer’s disease, although the methods of which are still poorly understood (MV, 2013). Alzheimer’s progresses slowly through distinguishable stages. These stages have been outlined in figure 1.1 along with the areas of the brain affected during these stages.
When compared to a healthy brain, a person’s brain suffering from Alzheimer’s shows significant reduction in size. The cerebral cortex (outside) is highly folded to increase surface area. The higher ridges are called gyri or gyrus (singular) and the low valleys or gaps are called sulci or sulcus (singular). In a healthy individual, the folds on the surface of the brain look very full and tightly packed together with small sulci and plump gyri. In an individual suffering from Alzheimer’s, the gyri are much smaller and appear wrinkly, and the sulci are much larger due to the damage and loss of nerve cells. As Alzheimer’s starts close to the hippocampus, This area will show a great reduction in size along with the rest of the temporal lobe. This reference will take you to a YouTube video of a dissection of a healthy individuals brain and a person who suffered from Alzheimer’s (dementia, 2015).
There is currently no cure for Alzheimer’s disease but there is medication available to help slow its progression. Acetylcholinesterase inhibitors are prescribed to Alzheimer’s patients. These drugs help prevent the break down of Acetylcholine in the synaptic cleft, allowing more of this neurotransmitter to bind to receptors on the post synaptic membrane. Acetylcholine is a very important neurotransmitter with many different functions. In the brain acetylcholine helps us to pay attention, sense things and learn. Alzheimer’s patients show reduced
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