The Hidden Truth on Debatable Essay Topics for College Students

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The Editing Essay Service Diaries

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Alzheimer disease - Progressive and Deadly Brain Disorder - Free Essay Example

Alzheimer disease is a progressive and deadly brain disorder, in which communication between cells are halted and eventually lost. It is the most common form of dementia, and in ~90-95% of AD cases affects those over the age of 65. As communication amongst neurons is lost, symptoms such as inability to recall memories, make appropriate judgment, and proper motor function are lost and worsen over time. Affecting an estimated 2.4 million to 4.5 million Americans, with the number predicted to double within the next few years, preventing the start of Alzheimer is vital. The brain is divided into three main portions: the cerebrum, the cerebellum, and the brainstem. Though a single organ, each portion is further broken down into sections with distinct control in specific skills. The area most affected by AD is the cerebrum, which is divided into five lobes: frontal, parietal, occipital, temporal, and insula. Each lobe has control over various functions such as memory, voluntary motor functions, different senses, and processing. These actions are conducted through signaling between neurons. These nerve cells contain properties like excitability, conductivity, and secretion. Communication amongst neurons is vital for proper functioning of the whole body. In a healthy neuron, communication is conducted via neurotransmitters. A presynaptic neuron will release neurotransmitters resulting in the postsynaptic neuron responding to the message. Depending on the location of these nerves in the brain will result in whichever action is taking place. It is the prevention of proper signaling within the brain and cell death that leads to loss of function throughout the body, and ultimately to AD. Two major contributors to the progression of Alzheimer Disease are the production of beta-amyloid plaques and neurofibrillary tangles. Amyloid Precursor Protein (APP) is believed to assist in neuronal growth and repair. As persistent use is continued, it is potentially broken down and recycled. Alpha-secretase cuts the extracellular portion of APP while gamma-secretase makes its cut in the membrane of the neuron, resulting in a soluble fragment of APP. The creation of beta-amyloid plaque begins when beta-secretase joins alpha-secretase and gamma-secretase in the process of breaking down APP. Beta-secretase creates an addition cut leaving behind an insoluble monomer, amyloid beta. With the characteristic of being sticky, these fragments join together resulting in beta-amyloid plaques. These clumps block signaling at the synaptic cleft, preventing neurotransmission. These plaque buildups trigger an immune response leading to swelling of the brain causing damage to nearby neurons. They also make amyloid angiopathy deposits around blood vessels causing a weakening in the vessel walls. This could lead to hemorrhaging and blood loss. Neurofibrillary tangles are also extremely prevalent in AD patients, resulting in the degradation of microtubules within the neuron. With the buildup of beta-amyloid plaques, this initiates pathways within the neuron leading to the activation of kinase. Kinase transfers phosphate groups to the tae proteins; this alters the shape of tau protein. A change in shape means a change in function, so tau protein no longer binds the microtubules; they instead get tangled with each other, and the microtubules fall apart. With signaling unable to occur, affected neurons undergo apoptosis. As the number of neuronal deaths increase, large scale changes in brain take place. The brain atrophies with the gyri narrowing. As this occur, the sulci widen and the ventricles become larger. To discuss these alterations without the details, if one was to view a segment of a brain affected by Alzheimer disease, there would be two common characters: beta-amyloid plaques and tangles. The formation of the plaque originates from portions of the neurons of the brain. On a normal functioning neuron, amyloid-precursor proteins (APP) stick out through the cells membrane. Enzymes swing by and chop off the beta-amyloid protein fragment, leaving a somewhat sticky snippet behind. As more enzymes chop off more beta-amyloid proteins from neurons, these sticky fragments begin to clump together along with other molecules resulting in beta-amyloid plaque. It is thought that these plaques block cell to cell communication between neurons; it is also thought that they activate an immune response. This would explain the swelling of the brain and the damage done to affected neurons. Neurofibrillary tangles are another common theme to AD, but they occur within the neuron. The microtubules in the neuron are bound by tau proteins allowing for the transport of nutrients and messages to adjacent neurons. In AD, these tau proteins are chemically altered, and they no longer want to stabilize the microtubules. They begin to pair with other tau proteins and get tangled. Since the microtubules are no longer bound by the tau proteins, they fall apart and disrupts the transport of materials. There are two forms of Alzheimer: familial (early-onset) and sporadic (late-onset). Both types of AD form differently on a molecular level, though they result in the degradation of proper mental function (7). Familial has the deterministic genes, meaning that it is guaranteed to develop the disease if the the mutation in the gene is inherited. Mutations in these specific genes lead to an overproduction of APP in the brain and potentially to excess beta-amyloid plaques, thus interfering with vital regulation pathways of the brain. Sporadic AD have risk genes; these genes do not directly cause the disease, but they put an individual more at risk of developing AD. Sporadic is more common, consisting of the majority of Alzheimer cases (~90-90%) (7). There are no known genetic mutations that cause late-onset; however, researchers believe that cognitive function decreases with old age without any underlying reason. Certain inherited alleles have been thought to increase ones risk. APOE e4 has been linked to the higher chance of developing AD, but not all people who have the allele develop AD; likewise, not all people with Alzheimer inherited a copy of the allele. Familial Alzheimer begins to appear as early as the mid-30s up to 65. This type of AD is inherited in an autosomal dominant pattern, which is significantly less common than sporadic AD (1). Though rare, early-onset is better understood on the genetically inherited component. Three genes have been identified that lead to early-onset when a mutation occurs that normally function in certain brain housekeeping: PSEN-1 (chromosome 14) and PSEN-2 (chromosome 1) (1). Presenilin-1 (PSEN-1) is a subunit of gamma-secretase (4). Early-onset AD due to mutation of PSEN-1 is the most common form of early-onset, and 150 mutations have been identified (4). Mutation of PSEN-1 affects gamma-secretases ability to make its cut in APP in the accurate location (4). Presenilin-2 (PSEN-2) normally assists proteins in the transmitting of chemical signals from the membrane to the nucleus followed by the nucleus activating genes for further cell function (5). PSEN-2 also processes APP. Researchers have found a bout 11 mutations on PSEN-2; however, there are two specific mutations in the amino acids that make up PSEN-2 that are most commonly seen in early-onset (5). At position 141, asparagine replaces normal isoleucine, thus mutating PSEN-2 (5). The second mutation is located at position 239 where methionine replaces normal valine (5). Mutations in any of the amino acids used to make PSEN-2 disrupt APP processing which leads to the overproduction of amyloid beta peptide, thus resulting in amyloid clumps and damaging brain nerves (5). Fig. 1. Effect of AD on neurons. Fig. 1. AD causes neuron damage and death due to amyloid clumps and tau tangles Late-onset Alzheimers does not have a definite known gene to directly cause the disease; however, a combination of risk genes, lifestyle choices, and environmental influences are all factors that contribute to the development. Apolipoprotein E (APOE) gene located on chromosome 19, is the known risk gene (6,7). Various alleles aid in the age in which symptoms begin to show. APOE e2 is more rare, and it is thought to provide some protection, allowing AD to develop later in ones life (6). APOE e3 is the most common, but it does not increase or decrease the risk (6). APOE e4 increases the risk as well as lowers the age of when symptoms start to show (6). The more APOE e4 alleles one inherits, the higher at risk they are. There is not a cure for Alzheimer disease, nor are there any preventative measures that would reduce the risk of developing the disease. Through clinical studies, factors that decrease ones risk include not having a family history, being male, obtaining more years of education, and having good cardiovascular health by having a healthy diet and exercising regularly (6). Factors that increase ones risk are having a family history of Alzheimers, being female, having fewer years of education, and being in poor cardiovascular health (6). Older age also increases risk; by age 80, ones risk for developing AD jumps to 50%. Many research projects are underway to find a cure or find preventative measures that could delay development or reverse the process. Because of the rarity, there are no major studies conducted for early-onset Alzheimers due to lack of funding and volunteers who may be at risk. As life expectancy continues to increase, so does the number of patients affected with AD. Organ izations encourage volunteers, both healthy and at risk, to take a stand against Alzheimers by participating in clinical studies where hopefully someday, we will be without it.

A Tale to Tell - Why Your Narrative Essay is So Important

A Tale to Tell - Why Your Narrative Essay is So ImportantThe narrative essay is a college-level topic and one that some instructors and writers will look for when evaluating your writing. To help you in understanding how the essay works, here is a list of traits of a good one.First, it should be a good topic. If you've never written an essay before, it is highly recommended that you read a sample of an essay before doing so. This is not to say that you can't write an essay based on a sample.In addition, the topic should be interesting. Think about what makes you interesting, or, what gives you the passion for writing. Knowing this will make it easier to figure out the kind of topic that will make it work. An assignment in a class you might not get enough time in class will help you find the topic of a good narrative essay.Second, the topic should be divided into several different parts. Many students don't know how to do this, so they write a whole essay, but then break it up into se veral parts. This is usually a mistake because it does not flow well. You should make it flow well.Finally, the essay doesn't flow well if it is to be understood easily. Make sure that the sentences flow well, and that each sentence is clearly and easily understood. This is very important when a reader reads a large amount of words on a page.Here is a good list of traits of a good story. Read them carefully, and compare them to the traits of a good narrative essay. If you feel that you have written a good one, you can move onto some of the other characteristics. If you are unsure, consult with a professional first.At this point, you should be confident in your writing ability and the subject matter of your essay. In fact, you should already know how to write well. What you should know is how to tell a good story with strong information and narrative content.