Alzheimer’s Disease
INTRODUCTION
Alzheimer’s disease is a progressive degenerative disorder of insidious onset, characterized by memory loss, confusion, and a variety of cognitive disabilities. It is the major cause of dementia in the elderly and is characterized by the presence of neuropathologic lesions including: neurofibrillary tangles in the neuronal perikarya and in pyramidal neurons of the hippocampus, entorhinal cortex and neocortex, nucleus basalis of Meynert, and periaqueductal gray. Neuritic (senile) plaques often with a central or core deposition of amyloid within the plaque and in some cases with amyloid infiltration of blood vessel walls (amyloid angiopathy) and the adjacent perivascular neuropil; loss of neurons,
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DIAGNOSIS
Unfortunately the most accurate diagnosis of Alzheimer’s disease is by postmortem examination of the brain. The disease itself is not well defined, and its varied yet subtle manifestations lend difficulty in distinguishing it from other nervous system diseases or dementia-causing diseases. The danger exists that appropriate therapy that might bring relief or even cure, might be withheld from some patients if their conditions are misdiagnosed. Because, even though no effective treatment for AD is available, there are useful therapies for various diseases that produce symptoms of dementia (4).
The fact that AD usually develops later in life again complicates the boundaries of this disease. Because the process of normal aging is not completely understood, there are no consistent, established values of what constitutes "normal" cognitive impairment and memory loss with advancing years. Furthermore, the neurochemical changes, the neurophysiological changes, or the gross and fine anatomical changes that accompany normal aging are not understood well enough to provide a firm basis for determining "abnormal" changes. The brain of an 80 year old patient with AD may be difficult to distinguish from that of an age-matched normal patient without dementia. Also, some elderly patients have few or no senile plaques or neurofibrillary tangles. Even at earlier ages, the neurofibrillary tangles and senile plaques that
Alzheimer's and dementia is one of the many diseases that affects the nervous system, particularly the brain. Acute memory loss is known as dementia. Thus, Alzheimer's is a severe form of dementia. The diagnosis is the brain lacking brain cells and connections due to degradation. Symptoms of Alzheimer's includes memory loss which can range from minor to severe as well as confusion which directly corresponds to memory loss. Groups of nerves work together to focus on specific jobs such as communication and memory. The brain cells work together and “receive supplies, generate energy, construct equipment and get rid of waste.” Alzheimer's is believed to prevent parts of the cell to not function properly. Scientists are not thoroughly sure where the cells malfunction begins. As the cell continues to divide and spread, the infected cells begin to die off leading to damaged brain connections. Scientists believe that plaques and tangles are the cause of the disease. Plaques are “deposits of a protein fragment called beta-amyloid that build up in the spaces between nerve cells.” Tangles are “twisted fibers of another protein called tau that build up inside cells.” Age results in developed plaques and tangles though, Alzheimer patients have an abnormal amount of these
Alzheimer’s disease (AD) is a progressive and fatal form of dementia, frequently seen in the elderly altering their cognition, thought process and behavior. AD is reported in about half of patients that have a dementia diagnosis; one study states that about 10.3% of the population over 65 years is affected by dementia with an increase to almost 50% over the age of 8 (Beattie, 2002). Alzheimer’s disease is not a normal part of the aging process in humans, but rather found in a group of diseases that affect the brain leading to a decline in mental and physical control. AD when diagnosed has a very slow and gradual course, initially affecting the individual’s short term memory (Beattie, 2002). Alzheimer’s disease is the 6th leading cause of death, affecting more than five million people in the United States and is also one of the most common forms of dementia. Dementia can be defined as a disorder of progressive cognitive impairment severe enough to affect daily functions of an individual’s life (Fillit, et al., 2002).
Alzheimer’s disease (AD) is the most common form of dementia known today. The term “dementia” refers to a variety of conditions that arise from the loss of nerve cell function and/or nerve cell death in the brain, including Alzheimer’s disease, vascular dementia, Parkinson’s disease, Creutzfeldt-Jakob disease and other types of mixed dementia. Although all types of dementia arise from neuronal damage and/or death, each form of dementia is associated with distinct brain abnormalities and symptom patterns. Once a patient has been diagnosed with dementia, a physician must conduct further tests in order to determine the exact form of dementia that is present. Recent research indicates that many individuals,
In 1984 the criteria for diagnosing Alzheimer’s was developed by the Alzheimer’s Association. These three levels of diagnostic certainty were: Possible, Probable, and Definitive. In the Possible AD level, symptoms were not typical, but other disorders were ruled out. For example, it could be diagnosed if the patient had another illness, as well as with symptoms of dementia. The next level is Probable AD. In this level of criteria, the diagnostic evaluation excludes other causes of diagnostic decline. In addition to this, the historical pattern of functional and behavioral disturbances was noted. With these techniques, doctors were able to diagnose with an 85-95% accuracy. The last level was called Definitive AD. Within in this level, an autopsy was performed and the examined brain tissue revealed
Alzheimer’s disease (AD) is a progressive and fatal form of dementia, frequently seen in the elderly altering their cognition, thought process and behavior. AD is reported in about half of patients that have a dementia diagnosis; one study states that about 10.3% of the population over 65 years is affected by dementia with an increase to almost 50% over the age of 85. (Beattie, 2002) Alzheimer’s disease is not a normal part of the aging process in humans, but rather found in a group of diseases that affect the brain leading to a decline in mental and physical control. AD when diagnosed has a very slow and gradual course, initially affecting the individual’s short term memory. (Beattie, 2002)
Alzheimer’s disease (AD) is a form of dementia that causes problems with memory, thinking, and behavior. AD typically involves the development of a progressive neuropsychiatric disorder that is characterized by gradual memory impairment, loss of acquired skills and emotional disturbances (Lee, Y. J., Han, S. B., Nam, S. Y., Oh, K. W., & Hong, J. T.). Every 67 seconds an individual in the United States develops AD. AD is the sixth leading cause of death in the United States. There are 5.3 million Americans diagnosed with AD (Latest Alzheimer's Facts and Figures). AD is one of the few degenerative diseases that cannot be prevented, stopped, or cured (Latest Alzheimer's Facts and Figures). Post-mortem examination of the brain of AD patients usually
Alzheimer’s disease, also referred to as AD, is a form of dementia that affects millions of people worldwide. AD is best known for causing memory loss in those who suffer from it, as well as affecting decision-making, language, and decision making progressively over time (Zou et at, 2014). According to Zou et el (2014), the symptoms of AD are caused by a build of plaques in the neurons of the brain. Alois Alzheimer discovered the disease, which was later named after him, when a woman at the age of 51 presented to him with a case of dementia that was new to him. Alzheimer was able to deduce the behavior of the woman with certain cognitive features, as well as through autopsy proceedings, that the symptoms were caused by “senile plaques” within
Alzheimer’s Disease is a disease of the future. With the growing aged population, this disease, which affects primarily the elderly, will become of increasing relevance to the medical profession. Also, the high frequency of Alzheimer’s, and the high cost in labor, money, and material of caring for its victims shall put considerable burden on the society as a whole. Here, however, these issues are not going to be debated. Instead the pathology of Alzheimer’s will be reviewed to the extent it is known today.
Alzheimer disease (AD) is the most common cause of dementia in the elderly, accounting for 65–70% of all cases (Jellinger, Janetzky, Attems, & Kienzl, 2008). The other dementias are of the Parkinson 's group, the fronto-temporal group and the vascular group. The total worldwide yearly costs for the treatment and care of patients suffering from dementia are estimated to be around 250 billion US dollars. The lifetime risk for AD between the ages of 65 and 100 is 33% for men and 45% for women with an annual increase of 1–2% in the seventh decade to almost 60% in the 10th decade with doubling every 5 years (Jellinger et al., 2008). AD is incurable, and thus represents a major public health problem. AD represents a challenge to humanity due to its relatively recent discovery, progressive nature of the illness, and complex diagnosis.
The disease called Alzheimer’s is the fourth leading cause of death in the United States (Weiner, 1987). It is estimated that the elderly population will double between now and 2030. During this period, the number of elderly will grow by an average of 2.8% annually (U.S. Census Bureau, 2001). By 2050, the number of people with Alzheimer’s is estimated to range from 11.3 million to 16 million (Alzheimer’s Association, 2005). These startling numbers should prompt an examination into one of the leading causes of death among this group of people. Understanding what Alzheimer’s is and the known causes of the disease are a good starting point. For those who have aging family members, knowing the risk factors and warning
With the growing number of people becoming diagnosed, and experiencing symptoms of Alzheimer’s disease, we must begin to take precautions and somehow attempt to gain knowledge of how the disease can be better treated, and ultimately prevented.
The research into Alzheimer's Disease has come a long way since 1906 when it is was discovered by Alois Alzheimer. He detected microscopic brain tissue changes called senile and neuritic plaques in deceased patients. These are chemical deposits consisting of protein molecules called Amyloid Precursor Protein(APP) that are fundamental components of a normal brain. However in the brain of an Alzheimer patient, an enzyme cuts the APP apart and leaves fragments in the brain tissue. These combined with degenerating nerve cells cause the plaques or lesions. These lesions are found in many sections of the brain including the hippocampus which regulates emotion and memory, the basal forebrain, and especially the basal nucleus of Meynert and the cortex, where the memory function is located.(2) Another sign of a diseased brain are neurofibrillary tangles, which are malformations within nerve cells.
Another clue may be the effects the aging process has on the brain as it is harming the neurons in the brain causing the disease (NIA, 2012). Regardless of the cause, AD is a life altering disease in every aspect of the victim’s life.
Alzheimer's disease is a chronic, neurodegenerative disorder that attacks the brain’s neurons, resulting in loss in memory, destruction of thinking and verbal skills, and changes in behavior (Kerr & Small, 2005). It is known as the most common factor of promoting dementia after the age of 65. Besides, the estimation of dementia sufferers is 24 million people in the beginning of 21st century, and it is assumed that the figure may rise threefold by 2040 (Kawas, 2003; “The three stages of Alzheimer's disease”, 2011). This essay will discuss biological features of Alzheimer's disease in neurological, cortical and physiological perspectives. It will then evaluate how the progressive damage that may lead to cognitive impairment. Finally, some
AD victims show clear structural abnormalities with the loss of neurons that liberate acetylcholine from a brain region called the nucleus basalis, beta-amyloid plaques, clusters of abnormal proteins deposited outside neurons, and the neurofibrillary tangles, abnormal bundles of protein filaments inside neurons in affected brain regions. (Patents, 2015) As we age the protein called beta-amyloid and tau begins to accumulate in the brain, causing the accumulation of beta-amyloid protein in plaques that causes the nerve cells to die. (Patents, 2015) Beta-amyloid is a solitary molecule that travels freely in the brain, but as we age the molecule begins to bunch up into small clusters and finally the plaque forms into clusters that form, beta-amyloid that bind to a receptor on nerve cells, setting in motion a process that erodes nerve cells. (Patents, 2015) This stage is called the presymptomatic stage as more and more beta-amyloid plaques and neurofibrillary tangles form in the brain, healthy neurons begin to work less efficiently, and their ability to correctly function, communicate and eventually die. (Patents, 2015) This process begins in the