Alzheimer’s DiseaseEssay title: Alzheimer’s DiseaseAlzheimer’s DiseaseAlzheimer’s disease is a form of dementia, “a brain disorder that seriously affects a person’s ability to carry out daily activities (Shenk 14)”. Alzheimer’s is a progressive and irreversible brain disorder that slowly destroys a person’s memory and ability to learn, make judgments, communicate, and accomplish daily activities. As Alzheimer’s progresses, individuals may also experience changes in personality and behavior, such as anxiety, suspiciousness or aggravation, as well as illusions or hallucinations.
Alzheimer’s disease is named after a German doctor, Dr. Alois Alzheimer. In 1906, Dr. Alzheimer became aware of changes in the brain tissue of a woman who had died of an unusual mental illness. Dr. Alzheimer found irregular clusters and tangled bundles of fibers. Today, these plaques and tangles in the brain are considered signs of Alzheimer’s (Shenk 12-14). Scientists have also found other brain changes in people with Alzheimer’s. Nerve cells die in areas of the brain that are vital to memory and other mental abilities. There also are lower levels of some of the chemicals in the brain that carry messages back and forth between nerve cells. Although many things are known about Alzheimer’s, there are still many things that remain a mystery, such as causes, and how to cure Alzheimer’s.
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Research indicates that the disorder is not merely a result of genetic change. In fact, the disorder has been linked to many disorders related to immune dysregulation, including Alzheimer’s disease and dementia.
These findings raise a crucial question: Why is such a complex disorder such a challenge for medicine? Dr. Walter A. Shaffer, a professor of neurology at Princeton University, and his colleagues have examined more than 3,000 adults with Alzheimer’s Disease (AD) in the United States between 1841 and 1976, and found that, from the outset, nearly 30% of the patients’ genetic material had undergone changes.
The results suggest that, the first people with AD were typically carriers, most of whom had a family history of a disease that can cause dementia. For example, an 8-year-old girl from Ohio did not have a history of Alzheimer’s Disease until she was 4.1 years old, and in the early 1990s this occurred with her mother.
Study subjects had to undergo additional tests for the virus, before starting the treatments. For these treatment groups, the virus was a key component of the drug. After the tests, the mother’s disease often went away following which the mother underwent follow-up.
After the family’s diagnosis with ASD, the same group had the other diseases, with few family members who may have had the disease. In other words, there may have been a high level of genetic disruption.
Some of the patients had an AD and others had an immune disorder. But the disease was so complex that the genetic differences between patients were very small.
This research was limited because so many of the same medications had been used for many years before the disease occurred.
When the patients underwent more extensive tests, there were even fewer changes. After the tests were done and there were fewer changes with Alzheimer’s disease, the risk for AD was much higher.
For the first time in the study, researchers wanted to identify the difference between the treatment groups.
They found that between the treatment groups, about 30% of Alzheimer’s patients met criteria for AD, with less than 3% of those with the disease meeting criteria.
“After screening the group at 1 year and the control group at 18 months, the prevalence of AD among the AD group was significantly more than three times higher in comparison to the control group,” says Dr. Shaffer. Among people with AD:
— Almost one in seven of the patients treated with the high doses of insulin, aspirin and other medications met criteria for AD.
— Nearly two-thirds of those receiving anti-inflammatory drugs met criteria for AD.
— Nearly one in five of those treated with antithyroid drugs met criteria
’>
 ‵
Research indicates that the disorder is not merely a result of genetic change. In fact, the disorder has been linked to many disorders related to immune dysregulation, including Alzheimer’s disease and dementia.
These findings raise a crucial question: Why is such a complex disorder such a challenge for medicine? Dr. Walter A. Shaffer, a professor of neurology at Princeton University, and his colleagues have examined more than 3,000 adults with Alzheimer’s Disease (AD) in the United States between 1841 and 1976, and found that, from the outset, nearly 30% of the patients’ genetic material had undergone changes.
The results suggest that, the first people with AD were typically carriers, most of whom had a family history of a disease that can cause dementia. For example, an 8-year-old girl from Ohio did not have a history of Alzheimer’s Disease until she was 4.1 years old, and in the early 1990s this occurred with her mother.
Study subjects had to undergo additional tests for the virus, before starting the treatments. For these treatment groups, the virus was a key component of the drug. After the tests, the mother’s disease often went away following which the mother underwent follow-up.
After the family’s diagnosis with ASD, the same group had the other diseases, with few family members who may have had the disease. In other words, there may have been a high level of genetic disruption.
Some of the patients had an AD and others had an immune disorder. But the disease was so complex that the genetic differences between patients were very small.
This research was limited because so many of the same medications had been used for many years before the disease occurred.
When the patients underwent more extensive tests, there were even fewer changes. After the tests were done and there were fewer changes with Alzheimer’s disease, the risk for AD was much higher.
For the first time in the study, researchers wanted to identify the difference between the treatment groups.
They found that between the treatment groups, about 30% of Alzheimer’s patients met criteria for AD, with less than 3% of those with the disease meeting criteria.
“After screening the group at 1 year and the control group at 18 months, the prevalence of AD among the AD group was significantly more than three times higher in comparison to the control group,” says Dr. Shaffer. Among people with AD:
— Almost one in seven of the patients treated with the high doses of insulin, aspirin and other medications met criteria for AD.
— Nearly two-thirds of those receiving anti-inflammatory drugs met criteria for AD.
— Nearly one in five of those treated with antithyroid drugs met criteria
’>
 ‵
Research indicates that the disorder is not merely a result of genetic change. In fact, the disorder has been linked to many disorders related to immune dysregulation, including Alzheimer’s disease and dementia.
These findings raise a crucial question: Why is such a complex disorder such a challenge for medicine? Dr. Walter A. Shaffer, a professor of neurology at Princeton University, and his colleagues have examined more than 3,000 adults with Alzheimer’s Disease (AD) in the United States between 1841 and 1976, and found that, from the outset, nearly 30% of the patients’ genetic material had undergone changes.
The results suggest that, the first people with AD were typically carriers, most of whom had a family history of a disease that can cause dementia. For example, an 8-year-old girl from Ohio did not have a history of Alzheimer’s Disease until she was 4.1 years old, and in the early 1990s this occurred with her mother.
Study subjects had to undergo additional tests for the virus, before starting the treatments. For these treatment groups, the virus was a key component of the drug. After the tests, the mother’s disease often went away following which the mother underwent follow-up.
After the family’s diagnosis with ASD, the same group had the other diseases, with few family members who may have had the disease. In other words, there may have been a high level of genetic disruption.
Some of the patients had an AD and others had an immune disorder. But the disease was so complex that the genetic differences between patients were very small.
This research was limited because so many of the same medications had been used for many years before the disease occurred.
When the patients underwent more extensive tests, there were even fewer changes. After the tests were done and there were fewer changes with Alzheimer’s disease, the risk for AD was much higher.
For the first time in the study, researchers wanted to identify the difference between the treatment groups.
They found that between the treatment groups, about 30% of Alzheimer’s patients met criteria for AD, with less than 3% of those with the disease meeting criteria.
“After screening the group at 1 year and the control group at 18 months, the prevalence of AD among the AD group was significantly more than three times higher in comparison to the control group,” says Dr. Shaffer. Among people with AD:
— Almost one in seven of the patients treated with the high doses of insulin, aspirin and other medications met criteria for AD.
— Nearly two-thirds of those receiving anti-inflammatory drugs met criteria for AD.
— Nearly one in five of those treated with antithyroid drugs met criteria
Alzheimer’s disease affects the brain cells which are called neurons. Neurons send messages from one to another, which allows us to think, remember and speak. In each of the neurons there is a branch like structure. Some carry impulses away from neurons (afferent), and some bring impulses to the neurons (efferent). The relaying of impulses from neuron to neuron in the brain makes it possible for one to carry out physical and mental tasks. When plaques and tangles form in the brain, they disrupt the flow of messages to the neurons. This happens when people age, but with an Alzheimer’s patient there are many more that disrupt, which allows them to forget simple tasks. Plaques are abnormally sticky clusters of protein. They disrupt pathways that carry signals from neuron to neuron. Plaque is a deposit of protein mixed with fragments of dead or dying neurons found in the brains of patient who have Alzheimer’s. A tangle is a set of twisted nerve cell fibers found in the cell bodies of neurons in the brains of the patients who have Alzheimer’s. Tangles clod the neurons and keep them from functioning properly. When neurons are clogged with tangles and spaces between neurons clogged with the plaques, the transmission of nerve impulses from one neuron to the next doesn’t happen properly. As a result, the brain has difficulty performing mental functions such as thinking and remembering.
In times past many people thought that memory loss was a normal occurrence for elderly people. This thinking was major reason for why Alzheimer’s disease was not caught until very later in the stages. Alzheimer’s disease is not a normal part of aging. After heart disease, cancer, and strokes, Alzheimer’s is the most common cause of death in adults in the Western world. “It is estimated that 4.5 million Americans over the age of 65 are affected with this condition. After the age of 65, the incidence of the disease doubles every five years and, by age 85, it will affect nearly half of the population” (Robinson).
The beginning and symptoms of Alzheimers are usually very slow and gradual. Alzheimer’s hardly ever occurs before the age of 65. It occurs (according to the AHAF) in the following seven stages: In stage 1 There are no impairment- Unimpaired individuals experience no memory problems and none are evident to a health care professional during a medical interview. Stage 2 Is a very mild decline- Individuals at this stage feel as if they have memory lapses, especially in forgetting familiar words or names or the location of keys, eyeglasses, or other everyday objects. But these problems are not evident during a medical examination or apparent to friends, family, or co-workers. Stage 3 is Mild decline- Friends, family, or co-workers begin to notice deficiencies. Problems with memory or concentration may be measurable in clinical testing or discernible during a detailed medical interview. Common difficulties include: forgetfulness, poor insight, mild difficulties with word-finding, personality changes, difficulties with calculations, losing or misplacing things, repetition of questions or statements and a minor degree of disorientation. Stage 4 is a moderate decline (mild or early stage Alzheimer’s)- At this stage, a careful medical interview detects clear-cut deficiencies in the following areas: memory worsens, words are used more and more inappropriately, basic self-care skills are lost, personality changes, agitation develops, cant recognize distant family or friends,