Alzeihmer's Disease Explanation - Essay Example

Running Head Alzheimer's disease Alzheimer's Disease 2007 Table of Contents Introduction 3 2. Clinical Features: Stages and Manifestations 3 a. Definition of Alzheimer's Disease 3 b. Definition of Dementia 4 c. Depression and other psychiatric conditions 4 3. Pathology 4 i. Causes of the disease 4 ii. Genetic factors 5 4. Diagnosis 5 a. Symptoms 5 b. Risk Factors 6 5. Treatment 7 a. New approaches 7 b. Future Perspectives 8 6. Conclusion 9 7. References 10 Alzheimer's Disease Alzheimer's disease is the most common neurological disease that causes dementia, a syndrome characterized by loss of intellectual capacities and impairment of social and occupational functioning. The incidence of the disease in women is higher than in men. The disease knows no socioeconomic boundaries. Life expectancy is reduced by approximately one-third after development of Alzheimer's disease. People with Alzheimer's disease live an average of 8 to 10 years after diagnosis. The disease can last for up to 20 years. The rate of deterioration and severity varies. Alzheimer's is a disease of the brain that causes a gradual but progressive loss of abilities in memory, thinking, reasoning, judgment, orientation, and speech. It causes an inability to recognize and identify objects and carry out motor activities. People with the disease are eventually unable to perform the most basic activities of daily living such as dressing, cooking, and bathing. Alzheimer's disease is not the result of normal aging, but it does occur more frequently in those 65 years of age or older. Alzheimer's disease is far more serious than the occasional forgetfulness experienced by the elderly. In its early stages, however, the disease may be difficult to distinguish from ordinary forgetfulness. Because the disease affects the brain gradually and persons ordinarily will compensate for the early symptoms, neither the person with Alzheimer's disease nor those around them may suspect a real problem at first. The results of Alzheimer's slow but progressive damage to the brain may not be noticed until the person experiences greater than normal life stressors, major health problems, or a situation that stretches coping abilities to the breaking point; or until major behavior problems, a driving accident, unpaid bills, or significant changes in daily functioning make denial or avoidance of what is happening impossible (Alzheimer's Disease 2007). Dementia, in its broader sense, indicates a loss or impairment of a person's abilities to use his or her mind. The essential feature of dementia is a loss of intellectual abilities severe enough to interfere with social or occupational functioning. An accountant with Alzheimer's disease will be unable to perform her job because of impairments in memory, reasoning, and calculation abilities. A farmer will become unable to plant and harvest crops. Buying seed and figuring out how much seed to put in planters or drills will become impossible. Although Alzheimer's disease is the most common type of dementia, it is not the only 'dementing' illness. Multiple strokes can cause a dementia that resembles Alzheimer's disease. Vascular dementia is the second most common type of dementia (Early Diagnosis of Dementia. Paper 2007). When vascular dementia and Alzheimer's are present, stroke damage can make symptoms of Alzheimer's disease more severe. Following Payne (1998) Alzheimer's disease has more closely examined other conditions that cause dementia. Some are not frequently discussed; others will become more familiar and possibly diagnosed more often. The growing focus on other diseases that can cause dementia is expanding our understanding of Alzheimer's disease. Harris and Sterin (1999) explain that depression and other psychiatric conditions can appear to be the results of dementia. In the elderly, severe depression may resemble dementia. This condition used to be called pseudodementia or "false" dementia. When severe depression is thought to cause impaired memory but memory does not improve with successful treatment of depressive symptoms, some type of dementia is probably developing. Researches (Freeman, 2003; Melton, 2000) has made considerable progress toward understanding the disease. Following Meyer (1998) Alzheimer's disease is not a simple disease with one obvious cause. It is a complicated disease that develops as the result of a complex cascade of events that occur over a period of time and affect the brain. Alzheimer's disease results from a combination of genetic and environmental factors, as well as from other factors that are being identified. Nongenetic factors such as the free radical damage linked with oxidative stress, disease-related brain inflammation, and damage associated with brain infarcts are believed to play a role in the development of the disease. The multiple genetic and nongenetic mechanisms through which the disease develops demonstrate the difficulties researchers face in identifying a clear-cut cause that points to one definite treatment. According to Freeman (2003): "forms of A[beta] known as A[beta]-derived diffusible ligands, or ADDLs, may, along with senile plaques, play a key role in the pathogenicity of Alzheimer disease" (p. 45). Genetic factors are certainly involved in the disease, but Alzheimer's is a genetically complex and heterogeneous disease. Only a small percentage of Alzheimer's disease cases are actually caused by genetic defects. Genetic defects on three chromosomes-21, 14, and 1-are known to cause early-onset Alzheimer's in a small number of families. The disease occurs before age 60 in these individuals (Alzheimer's Disease 2007). According to Phelps (2005) the most common form of Alzheimer's occurs in persons who are 65 and older and thus it is called late-onset. One study suggest that the increased incidence of Alzheimer's in older women may be due to estrogen deficiency. Estrogen replacement therapy may be useful for preventing or delaying the onset of Alzheimer's disease. The diagnostic criteria for dementia of the Alzheimer's type stipulate symptoms and how they can be recognized and measured by a person involved in the diagnostic process. "There is currently no single test to identify Alzheimer's disease. The diagnosis is made only after careful clinical consultation" (Alzheimer's Disease 2007). Multiple cognitive deficits must have developed and be manifested by both (1) memory impairment and (2) one or more of the following cognitive disturbances: aphasia, apraxia, agnosia, and/or a disturbance in executive functioning. Executive functioning refers to cognitive abilities that involve planning, organizing, sequencing, and abstracting. (Aphasia, apraxia, and agnosia are explained later in this chapter.) Other conditions must also be met. For instance, the course of the disease must be characterized by a gradual onset and continuing cognitive decline, and not be due to other known medical or psychiatric conditions. Personality changes occur with dementia. Usually these changes become evident after the very early stages of the illness. Alzheimer's disease is a probable diagnosis given only after all other potential causes of dementia have been identified and treated or ruled out. An individual's functioning and quality of life may improve by treating other health problems that coexist with Alzheimer's disease. Some medical tests have been developed to help diagnose Alzheimer's disease, but none are 100 % accurate. As the accuracy of diagnosis has improved and more attention has been given to mental status and performance of activities of daily living, the process of ruling out other conditions just to make the diagnosis of Alzheimer's disease is no longer necessary (Alzheimer Australia WA Ltd. 2007). Other possible conditions are always considered, but Alzheimer's is no longer viewed as a diagnosis of exclusion (Alzheimer Australia WA Ltd. 2007). Increasing age is the strongest risk factor for Alzheimer's disease. The elderly tend to get more autoimmune diseases such as cancer, late-onset diabetes, and rheumatoid arthritis. Other neurological diseases, including multiple sclerosis and Huntington's chorea, are known to involve immune system alterations; several studies report abnormalities of brain immune function may contribute to the progression of Alzheimer's disease. Also, regular psychical activity, diet (based on fruits and vegetables) and communication can reduce risks and factors of Alzheimer's disease (Mind Your Mind 2007). One of the most recent approaches to treatment is Memantine approach. Keltner and Williams (2004) explains: "Memantine is an N-methyl-D-aspartate (NMDA) receptor antagonist. Specifically, it blocks abnormal (i.e., sustained) signaling from glutamate neurotransmitters but does not affect the normal binding of this endogenous ligand" (p. 123). Researchers (Keltner and Williams 2004) suggest that Memantine slowed the progression of symptoms in persons with moderately severe to severe Alzheimer's disease. Compared to placebo, persons taking this substance manifested improvements in clinical global, cognitive, and behavioral functions. Medical treatment includes cholesterol reducing dugs and female hormone therapy, usage of non-steroidal anti-inflammatory drugs. Recent studies (Phelps, 2005) suggest that "transthyretin may block the progression of Alzheimer's disease by inhibiting the effects of [beta]-amyloid. This discovery suggests that it may be possible to develop a drug that increases the production of transthyretin and thus protects people at risk for AD, such as those with a genetic predisposition" (p. 67). The lecithin increased the availability of acetylcholine in the synapses between neurons, while the THA inhibited the activity of the enzyme that breaks acetylcholine down in the receiving neuron. Together they produced the desired effect: more usable acetylcholine in the brain. In another study, lecithin and THA were given together to a group of Alzheimer's subjects with relatively high education and an average age of 61.5 years; some improvement in learning was noted, particularly among the more mildly impaired. The lecithin increased the availability of acetylcholine in the synapses between neurons, while the THA inhibited the activity of the enzyme that breaks acetylcholine down in the receiving neuron. Following Hirai (2000), in the future, it may be possible to graft healthy neuronal tissue onto impaired areas of the Alzheimer's brain, thus stimulating the regeneration of neuron networks and improving certain brain functions. This transplant technique could offer an important alternative for more severely impaired persons, since drug therapies rarely seem to help those with extensive neuron damage. According to Melton (2000) the use of neuronal transplantation as a treatment for Alzheimer's disease is a growing possibility emerging from nearly two decades of research, particularly with Parkinson's disease. This treatment holds promise for other degenerative brain disorders such as strokes. Alzheimer's disease is a chronic inflammatory state that affects the brain and causes memory loss. Alzheimer's disease causes brain damage that results in a loss of neurons and neurotransmitters. These physical and chemical changes contribute to problems with mood, behavior, and cognition. A greater loss of neurons in some parts of the brain predisposes some individuals with Alzheimer's disease to depression. References 1. Alzheimer's Disease. (2007). Alzheimer's Australia Retrieved May 02, 2007 from www.alzheimers.org.au/content.cfminfopageid=439 2. Alzheimer Australia WA Ltd. (2007). Alzheimer's Australia. Retrieved May 02, 2007 from from http://www.alzheimers.asn.au/ 3. Early Diagnosis of Dementia. Paper No. 10. (2007). Alzheimer's Australia. Retrieved May 02, 2007 from http://www.alzheimers.org.au/content.cfminfopageid=3498 4. Freeman, K. (2003). ADDLs: A New Explanation for Alzheimer's disease. Environmental Health Perspectives, 111, 45-47. 5. Hirai, Sh. (2000). "Alzheimer's disease: Current Therapy and Future Therapeutic Strategies." Alzheimer's disease and Associated Disorders, 14, S11-S17. 6. Harris, P. B., and Sterin, G. J. (1999). "Insider's Perspective: Defining and Preserving the Self of Dementia." Journal of Mental Health and Aging, 5, 241-256. 7. Keltner, N.L., Williams, B. (2004). Memantine: A New Approach to Alzheimer's Disease. Perspectives in Psychiatric Care, 40, 123. 8. Melton, L. (2000, June 17). Neural Transplantation: New Cells of Old Brains. The Lancet, 355, pp. 2142. 9. Meyer, M. R. (1998). APOE Genotype Predicts When-Not Whether-One Is Predisposed to Develop Alzheimer disease. Nature Genetics, 19, 321-322. 10. Mind Your Mind. (2007). Alzheimer's Australia. Retrieved May 02, 2007 from http://www.gtp.com.au/alzheimer/inewsfiles/MYM_book_low_res.pdf 11. Payne, J. L. (Fall 1998). Relationship of Cognitive and Functional Impairment to Depressive Features in Alzheimer's disease and Other Dementias. Journal of Neuropsychiatry and Clinical Neurosciences, 10, pp. 440-447 12. Phelps, J. (2005). Neural Protein may Stop the Progression of Alzheimer Disease. Environmental Health Perspectives, 113, 67-68. Read More