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INTRODUCTION TO alzheimer's disease
Informative outline of alzheimers
INTRODUCTION TO alzheimer's disease
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Recommended: INTRODUCTION TO alzheimer's disease
Alzheimer’s disease, also known as irreversible dementia is a neurodegenerative disorder which progresses slowly over the years and ultimately leads to death of the person. Its symptoms include cognitive decline, forgetfulness, inability to recognize family members or carry out normal activities, depression, mood swings, lack of a coordinated muscle movement .In the later stages inactivity combined with appetite loss and weak immune state makes the disease a fatal one. Earlier it was believed to be an age-related decline in brain function but Dr.Alois Alzheimer’s report in 1906 proved that it was much more than just an age-related disorder. He observed the presence of plaques and tangles and also the disappearance of many nerve cells from the brain tissues he had studied1. These were believed to be the cause of Alzheimer’s disease. There are two types of Alzheimer’s disease: familial Alzheimer’s disease (FAD) which is a rare inherited form of Alzheimer’s disease and the more common, sporadic form of Alzheimer’s disease. FAD strikes a person at an earlier age but sporadic form shows up generally at the age of 65 or older. Summary: Changes taking place in an Alzheimer’s brain: 1) Formation of plaques: The plaques, observed by Dr.Alzheimer are actually made up of amyloid beta, in short Aβ protein which are derived from amyloid protein precursor (APP).Although Aβ and APP are present in healthy nerve cells, in Alzheimer’s brain it gets accumulated in humongous amounts which is due to either overproduction of Aβ or the failure of clearance mechanisms2. Also the blood vessels which picks up and removes A-beta proliferates and become leaky and hence cannot function properly3. But the real danger is not the individual A-beta molecules ... ... middle of paper ... ...asing the risk element. It also causes plaque and tangle formation and disrupts mitochondrial function and certain of the synaptic mechanisms involved in communication between nerve cells14. Hence the alternative could be to find more protective genes like ApoE2 and to always maintain a healthy lifestyle. 2) Other genetic variants acting as risk factors- i) People having FAD tend to have mutation in one of the three genes, namely the APP gene and two presenilin genes (PSEN-1 and PSEN-2).So it is highly likely that people who inherit these faulty genes will get the disease at an early age(30s or 40s)12. ii) A recently identified gene, GAB2 promotes the development of tangles15. iii) Four newly identified genes, CLU, PICALM, CR1, and BIN1 also acts as risk factors, probably by impairing the elimination of the excess Aβ protein, thus leading to its accumulation17.
Alzheimer’s disease was first defined in 1906 by a German psychiatrist, Alois Alzheimer. Alzheimer's disease is the most common form of dementia. It is a progressive brain disorder in which the nerve cells in the brain gradually die off. It is estimated that 26 million people world-wide are afflicted by Alzheimer’s and of those, approximately 4.5 million live in the United States. It is said to be the seventh leading cause of death in the USA and the fifth leading cause of death for those over age 65. Seventeen percent of women and ten percent of men age 55 and older can expect to develop Alzheimer’s (apa.org, 2009). Researchers report that this disease is more prevalent in African Americans and Hispanics than in whites (Crandell, Crandell, and Zanden, 2009, p. 578).
Alzheimer is a dementia type of disease named after Dr. Alois alzheimer that slowly destroys memory and thinking skills,and eventually , the ability to do simple things, or recognize their family. The first case occurred in the 1906 when a woman died on a unusual mental illness. After she died Dr.Alois examined her brain , amyloid plaques and neurofibrillary. Alzheimer’s is in older people the most common cause of dementia. Dementia is a loss of remembering ,thinking and reasoning skills, that intervenes with your daily life and activities. It is very common in people over sixty years of age. People younger than sixty years can also
Nerve cell death and tissue throughout the brain is the most significant affect over time. Naturally by age twenty-five the brain starts to decrease in size. With Alzheimer’s, the amount decrease is extremely significant. The cortex begins to shrivel up which is the part of the brain required for planning, remembering, and thinking. The most noticeable shrinkage occurs in the hippocampus. The hippocampus is responsible for the formation of new memories, it is also located inside the cortex. Upon further inspection under microscope, tissue samples are observed and synapses and nerve cell count is severely decreased. Tangles, are also found which our twisted strands of another protein due to nerve cells dying and bunching together. Plaques and tangles are prime suspects in the death and tissue loss in the Alzheimer’s brain. Beta-amyloid is a chemical and is sticky which causes it to gradually build up into plaques. This chemical derives from a larger protein found in the nerve cells with fatty membranes. These tangles destroy a vital cell transport system made of proteins.
Clinically, Alzheimer’s disease is characterized by the accumulation of beta-amyloid plaque between living neurons in the brain (Sabbagh, 2008). This results in an excessive calcium influx inside the neurons and the breakdown of a protein called tau. Normally, the rol...
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Alzheimer’s is a result from a combination of factors that cause progressive brain deterioration that affects the memory and behavior of an individual. There are two known risk factors. The first risk factor is age. Alzheimer’s usually affects people older than 60, and rarely affects those younger than 40. The average age
The first case of dementia was discovered in 1906 by a German physiatrist Alois Alzheimer. It was first observed in a female patient and she was forty-one years old her name was Auguste D. Dr. Alzheimer observed a decline in the patient’s cognitive abilities. She lost her memory, she exhibited behavioral issues, and she suffered from hallucinations, lost the ability to comprehend language, disorientation and lost her speech. After Augusta’s passing Dr. Alzheimer preformed an autopsy that showed the classic triangles and knots we associate today with Alzheimer. Those triangles and knots are a proteins and plaque. The brain is self looked smaller and had distinct characteristics. Still with modern medicine the only way to diagnose a person with Alzheimer is after their death with an autopsy. (THE ALZHEIMER'S PROJECT, 2014).
In this day and age, it seems as though almost everyone has experience a loved one taken away form a very serious disease known as Alzheimer’s disease. Alzheimer’s disease is unbelievably devastating for everyone affected by it. This disease is causing major economical problems such as less occupancy in the nursing homes, and hospitals due to the rising population of elderly men and women being diagnosed with it everyday. Because there is not yet a cure for this disease and the percent of the population being diagnosed keeps rapidly rising, more time and money needs to go towards Alzheimer’s research.
Alzheimer's Disease Introduction to Alzheimer's Alzheimer's disease is a progressive, degenerative disease of the brain. It was first described by the German neuropathologist Alois Alzheimer (1864-1915). in 1905. This disease worsens with advancing age, although there is no evidence. that it is caused by the aging process.
Alzheimer’s can be diagnosed before age 65, although rare, and is caused by a mutation in 3 known genes. About 5 percent of those who are under 65 and possess the ailment have AD in their family history. Given that the symptoms of AD are caused by plaque in the brain, causing loss of nerve cells that help the body communicate with the brain, mutations to these genes; amyloid precursor protein, presenilin 1, and presenilin 2 cause a excessive production of certain proteins (primarily a B-42 form of amyloid protein), and therefore spark an excessive growth of plaque cells which are toxic to the neurons of the brain. For those cases of Alzheimer’s that occur after age 65, a genetic mutation has yet to be proven, although some may be linked, to the fact that a difference may cause an increased chance of developing the ailment. Whatever the case may be for patients over 65 years old, the disease and its symptoms are caused by neurofibrillary tangles of almyloid plaques. It is impossible for someone to test positive for Alzheimer’s Disease, because the only way to determine an affirmative case i...
Since ancient times, it has been clear that some people lose mental sharpness (cognitive function) as they age. However, in 1906, the German neurologist Alois Alzheimer began an autopsy of a woman from Frankfurt, that had died after several years of progressive mental deterioration. From the accounts of the doctor, family, and friends of the woman, Alzheimer put together her mental state prior to death, and described the woman as being marked by increased confusion, disorientation, and memory loss.Taking advantage of staining techniques that had recently been established, Alzheimer noticed an odd disorganization of the nerve cells in the womanís cerebral cortex, the part of the brain...
Scientists know that Alzheimer disease is characterized by a gradual spread of sticky plaques and clumps of tangled fibers that disrupt the organization of nerve cells in the brain. However , a definite cause, prevention, or cause has not been found.
Thesis/Preview Statement – Alzheimer’s disease (AD) causes a decline in brain function, it destroys healthy nerve cells. Today, we have discussed Causes, Symptoms, and Diagnosis of AD.
Alzheimer’s disease or AD is an incurable disorder of the brain that results in loss of normal brain structure and function. In an AD brain, normal brain tissue is slowly replaced by structures called plaques and neurofibrillary tangles. The plaques represent a naturally occurring sticky protein called beta amyloid and in an Alzheimer’s brain, sufferer’s tend to accumulate too much of this protein. Neurofibrillary tangles represent collapsed tau proteins which, in a normal brain along with microtubules, form a skeleton that maintains the shape of the nerve cells. In Alzheimer’s disease, the tau proteins break loose from their normal location and form tangles. Without the support of these molecules, nerve cells collapse and die. As normal brain structure is lost with progression of the disease, brain function also degenerates. Patients afflicted with Alzheimer’s disease display a gradual mental decline. Initially, and most apparently, there is a loss of short-term memory. Eventually, as a patient progresses to later stages of the disease, the brain becomes so damaged that patients can no longer communicate or recognize immediate family or even themselves. They have difficulty walking and standing and frequently fall. In the final stages, they lose bladder and bowel control and have difficulty with swallowing, frequently leaving them malnourished and dehydrated. Eventually, they are forced to remain bedridden and, without the help of life-prolonging measures provided in a hospital, die. However, this level of deterioration is severe and may take as long as twenty years. Because of the disease’s slow progress and its usual later start in a person’s life, a victim of AD will usually die first of natural causes. Under the objectives ...
This usually occurs in older adults aged above 65; however, it is a disability and not a normal symptom of aging. Chances of inheritability are present, but it depends on the individual and the type of dementia (Alzheimer Australia, 2011). The Global Deterioration Scale provides a detailed explanation of the seven stages of cognitive decline in dementia (Alzheimer’s Association of Canada, 2005). Types of Dementia There are four main types of dementia, with AD being the most widespread form. It accounts for almost two thirds (50 -70 percent) of the cases and thus more extensively studied (Miller, 2009)....