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Alzheimer’s Disease

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Alzheimer’s disease is one of the forms of dementia, and has been discovered to be the most prevalent. It was discovered and explained by Alois Alzheimer, a German Psychiatrist and neuropathologist, in the year 1906, and since then, the disease has remained incurable, despite the developments. Alzheimer’s disease affects mostly aged people living past 65 years of age. A research conducted in 2006 showed that at least twenty six million people were suffering from the disease worldwide, and this figure keeps on growing.

This disease manifests itself differently in different people, but it is easy to generalize on some symptoms. The initial signs could easily be confused with old age-related problems. This is because patients experience the usual memory problems associated with old age. However, Alzheimer’s disease makes it difficult for patients to remember even recent events and places, and with time, this develops to frequent confusions, irritations which could even be aggressive and deterioration of the communication skills. Eventually, an individual’s body functions start being affected and leading to death.

Alzheimer’s disease develops in individuals for varying lengths of time before diagnosis, which are difficult to establish. Scientists have theorized that it could even be years. However, after diagnosis, the patients’ expectancy has been estimated to be seven years with less than three percent of them showing strength to live up to fourteen years (Alzheimer’s Association, 2011).

The full circumstances surrounding this disease, as well as causes, have not yet been fully understood. Scientists have related the disease to plaques and tangles of the brain. Currently, doctors just struggle with the symptoms, since there are no defined treatments that can stop or reverse the disease. Numerous researches on trials are underway, but with no concrete conclusions on which one will work.

In the explanation of the nature of this disease, it is necessary to understand that the brain contains about a hundred billion nerve cells usually referred to as neurons. These cells connect with each other to form the body’s communication networks. The brain also contains other cells, whose core function is nourishing and supporting other cells. The nerve cells also specialize in different jobs like memory, thinking, seeing, hearing and smelling among others. These cells can be likened to tiny factories which receive supplies and use them to generate energy, as well as build equipment to get rid of unwanted products. In addition, brain cells process and store relevant information, as well as communicate this information with other cells. These processes require high amounts of fuel and oxygen to burn it.

It is believed that Alzheimer’s disease affects the proper running of some cellular activities. Scientists have not discovered where the trouble begins, but, ideally, a breakdown in one of the processes causes failure in almost all cellular processes. This damage spreads slowly, impairing cells, and, eventually, killing them. Since the brain operates the entire body, impairment and death of brain cells are also expected to lead to malfunctions in body activities. These malfunctions begin with failure in the brain’s core activities, like thinking and storage of information. When it eventually advances to failure in body functions, then, the sufferer has little time left. The only help these people need is care, and, especially, from family members. The disease is known to be a burden not only to the patient, but also to caregivers.

This paper addresses how Alzheimer’s disease affects cellular processes in individuals, as well as what development scientists are currently making. Most importantly, the paper tries to answer the question of how to counteract the disease, as well as prevent it. The understanding of this disease is also expected to leave the reader in a better position to identify and deal with it.

The biochemistry of Alzheimer’s disease is a bit complicated and not well understood by scientists. However, this disease has been said to be a protein misfolding, a condition which is caused by abnormal accumulation of folded amyloid beta protein in the brain. It has been discovered through autopsies that the brain sufferers of Alzheimer’s disease contain a lot of plaques and tangles. Plaques are now those deposits of amyloid beta protein, also written as Aβ, which accumulate in between the nerve cells. It has also been discovered that these patients show accumulation of another type of protein known as tau, which forms twisted fibers referred to as tangles.

Generally, people develop these plaques and tangles, as they age, but patients of Alzheimer’s disease tend to deposit excess proteins (Pigino, 2009). These plaques and tangles have also been discovered to accumulate in predictable patterns in patients by beginning with areas responsible for memory and then slowly spreading into other regions. This can be one of the basic explanations of why these patients initially experience memory problems before advancing to other malfunctions of the body. However, the science of how these plaques and tangles hinder the functioning of neurons and, eventually, kill the cells, is not yet clear. It is just assumed that these protein deposits block or play a quite critical role in blocking communication between nerve cells. It is the general idea that even in normal factory operations, communication is vital, and its impairment leads to serious breakdowns in the entire operations. Therefore, it is only right to assume that failure of nerve cells to communicate with each other leads to disruption of all the other activities threatening the survival of the cell. The death of nerve cells is the reason for memory failure, changes in personality and all the other symptoms of Alzheimer’s disease.

There have been several other hypotheses explaining the cause of this disease apart from the amyloid hypothesis. For instance, initially, scientists advanced the cholinergic hypothesis, which blamed the synthesis of the neurotransmitter acetylcholine for Alzheimer’s disease. However, this theory could not gain much support worldwide due to ineffectiveness of the medication intended to correct acetylcholine deficiency. The amyloid beta protein hypothesis seems to have gained much popularity with more researches being based on that theory.

Scientists have so far discovered an experimental vaccine that successfully clears amyloid plaques in human beings. However, this vaccine fails to have significant effects on dementia. This has created different feelings among the researchers with some of the developing other hypothesis to explain the disease. There have been speculations of non-plaque amyloid beta oligomers, forming from the combination of many monomers, being the primary problem. These non-plaque amyloid beta oligomers, also referred to as ADDLs (amyloid-derived diffusible ligands), change the structure of the synapse in the nerve cells by binding the surface of receptors, thereby breaking the normal neural communication (Jellinger & Bancher, 2007). This makes these oligomers quite toxic, while in the brain, and entirely responsible for Alzheimer’s disease. This theory has been recently advanced to include another protein just closely related to amyloid beta, as also a key contributor to the cell communication breakdown.

Tangles, on the other hand, were introduced in the beta-amyloid hypothesis to explain the lack of correlation between amyloid plaques deposited and the loss of neurons. This development supported the tau hypothesis and brought two theories together, which enhanced their popularity. The tau protein abnormalities here also take some blame in causing of the disease. Ideally, hyperphosphorylated tau proteins pair with other threads tau proteins to eventually form the neurofibrillary tangles within the nerve cell bodies. This leads to the degeneration of the microtubules responsible for transportation in the nerve cells. First, cells experience malfunctions in the biochemical communication, and later, they die.

Other theories even claim that viruses, like the Herpes Simplex type one-virus, cause Alzheimer’s disease, with several scientists also being inclined to the notion that age-related issues of the brain like the myelin breakdown cause the disease. Scientists have also followed genetics in an attempt to find the cause of this disease, but they seem to agree that Alzheimer’s disease is a degenerative condition, rather than an inherited one. However, for the purpose of this study, we focus more on the protein misfolding problem, in order to explain the disease.

The accumulation of folded amyloid beta protein has been explained as follows: peptides form building bricks of plaques and are composed of 39 to 43 amino acids referred to as beta amyloid. This beta amyloid is just but a fragment of amyloid precursor protein, which is bigger in size, but with the capability to penetrate through the membranes of neurons. Amyloid precursor protein plays a key role in the growth of nerve cells, as well as their repair. For the patients of Alzheimer’s disease, amyloid precursor protein is broken down into fragments by enzymes in a process called proteolysis (Nixon, 2002). However, what makes these dangerous enzymes remains unknown, and still under speculations by scientists. Not all the fragments form plaques, but just one of them combining with each other from different molecules to form fibrils of amyloid beta and being deposited outside the nerve cells to become the plaques, also known as senile plaques.

One of the most current approaches to deal with Alzheimer’s disease symptoms makes use of the acetylcholine esterase inhibition or modification of the glutamate pathway. The acetylcholine esterase inhibition is adopted from the cholinergic hypothesis, which was explained earlier. Increasing acetylcholine levels, which is a significant neurotransmitter using therapeutic agents, like Donepezil, has helped many patients improve their neural activity, especially in the early stages of Alzheimer’s disease. The administration of Memantine has also proven to help many people with neurological disorders, including patients of Alzheimer’s disease. This drug acts as an antaonist in the channels of N-methyl-d-aspartate receptors. The ability to enhance communication between brain cells has proven to be quite helpful for patients of this disease, but it does not remedy the situation.

It is crucial to note that these medications were approved for their beneficial effect in slowing down the signs of Alzheimer’s disease, and not because they lead to cure. Doctors just give them to ease the symptoms, but they cannot entirely prevent, cure or reverse it. There have been several herbal treatments, but they usually rely on the above explained mechanisms and are clearly not as efficient as the chemical drugs.

This disease has attracted tremendous research by scientists, first in an attempt to explain what exactly causes the disease. Findings about circumstances surrounding the disease remain inconclusive and the disease’s nature to affect different people differently makes it extremely hard to predict its effects on an individual. Some researchers have likened Alzheimer’s disease to the mad cow’s disease, which has made cows reliable test subjects (Lott & Head, 2005). They have been studied for long to help unveil the real cause of Alzheimer’s disease, in order to establish its cure. This has also been one of the hardest puzzles for scientists, as what they seem to do is just treat the symptoms. There is no single drug that has helped an individual entirely out of this problem, even in its earliest diagnosed stages. Scientists are also focusing on proper diagnostic measures that can pinpoint a patient, even in the earliest stages possible before they show symptoms. This can help them use available therapies and medications combat the disease for a longer period.

Alzheimer’s disease has proven to be tough to crack, but the truth is that it attacks old people, especially, those living past the age of 60, and with a healthy diet, therapies and medication can be combated for up to fourteen years. This means that individuals can reach the 75 mark. Therefore, studies in the ways of combating these symptoms have helped greatly in reducing the risk posed by Alzheimer’s disease, and further careful analysis could help in equating this disease to simple old age conditions. The acetylcholine treatment, for instance, has helped many patients with this disease to keep up their neurological condition without worsening of symptoms for years. This shows that there is a lot of hope that future breakthroughs will even give the long awaited cure.

It seems that future investigations will be more inclined to plaques and tangles studies. These hypotheses have shown more light in the understanding of the disease, as well as combating symptoms. Scientists would now be interested in what causes the defragmentation of the amyloid precursor protein, in order to tackle the problem from the root. They should also be trying to come up with a better combination of therapies, medications and diets for patients of this disease to help sufferers live longer after diagnosis. This can be achieved through researchers coming together and sharing information on their developments concerning the disease. One should propose that more research should be done on the defragmentation of proteins without ignoring any genetic patterns as they could help find a solution.

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