Alzheimer’s Disease

Alzheimer’s disease is a progressive mental disease that occurs due to the degeneration of the brain. It can manifest itself in the middle and old age thus causing premature senility. An interest in the disease arises from the fact that the condition affects a person’s cognitive ability. It raises the curiosity of how the brain changes to the extent that a healthy a functioning brain ends up damaged and almost non-functioning. A person that was once healthy and active may have Alzheimer's disease, resulting in a loss of general body functioning. The cause of Alzheimer’s disease remains unknown although the early onset of the disease is associated with a genetic mutation. The late occurrence of Alzheimer’s disease, however, occurs due to a combination of genetic, environmental and lifestyle factors. People with APOE?4, have an increased of early onset of Alzheimer’s disease although people without the gene can also acquire the condition (Villemagne, & Ames, 2013).

Moreover, persons with Down syndrome have an increased risk of Alzheimer’s disease because of the existence of the extra chromosome 21 with the gene that produces the harmful amyloid. Conditions such as heart problems, diabetes, and high blood pressure have also been associated with a decline in cognitive functioning that increases the risk of Alzheimer’s disease. According to Qui & Strauss (2009), approximately 25 million people are affected by Alzheimer’s disease. In the Europe, the age-standardized prevalence in 65+ is 64% for dementia and 4.4% for Alzheimer’s disease. In America, the prevalence of Alzheimer’s disease in individuals over 70 years is 9.7%. The number of people who have Alzheimer's disease is anticipated to double in the next twenty years.

The first symptom for persons with Alzheimer’s disease is a cognitive impairment that begins to manifest through memory loss. The memory loss may not be immediate, but the individual may start by demonstrating increased forgetfulness and repetition of statements. The mild cognitive impairment may be difficult to detect, but as the condition progresses, it becomes obvious. The individual may demonstrate complete memory loss; he may wander and get the loss (Jack, 2013). The individual may also take longer to perform tasks that he used to take a short duration to complete. In the severest form of the condition, the individual loses the ability to communicate and may not recognize family members.

The symptoms begin and vary with the changes that the brain is experiencing. Alzheimer’s disease is progressive thus the damage to the brain can begin decades before the symptoms begin to show. The brain begins to have abnormal deposits of amyloid plaques and tau tangles (Selkoe, & Hardy, 2016). The result is the healthy neurons stop functioning and lose connections with each other. Damage first begins at the hippocampus, the part responsible for formation of memory. The damage to the hippocampus marks the indicator of the first sign of Alzheimer’s disease, memory loss.

The diagnosis of Alzheimer’s disease involves a variety of test, examination and a look at the individual history. A physician may also perform a variety of tests to measure the patients, memory, problem-solving abilities, and language capacity. Laboratory tests such as urine and blood tests may be performed to eliminate other diseases that may manifest similar symptoms. Moreover, a CT, MRI, and PET test may be performed to rule out other possible causes of symptoms. Conditions such as stroke, brain tumors, and Parkinson’s diseases can expose an individual to symptoms such as those of Alzheimer’s disease.

There is no single intervention that is suitable for the management of Alzheimer’s disease. A patient may require a diversity of drugs and intervention to manage the condition (Liu & Shen, 2014). Currently, the emphasis is on helping patients maintain their mental function, manage their behavioral symptoms, and slow down the progression of the disease. There have been intensive studies to develop therapies that target the genetic, molecular and cellular mechanism of the disease. Medication such as donepezil, rivastigmine, and memantine are given to manage mild to severe Alzheimer’s. The drugs work by regulating the neurotransmitters, maintain thinking, memory and the patient’s communication skills. The medication does not work for all patients, while for others it may work for a while before they no longer do.

Unlike factors such as age and genetics that may be uncontrolled about the occurrence of Alzheimer’s disease, lifestyle and health factors can be controlled. Exercise and physical activity can ensure a healthy brain as the activities encourage the formation of blood vessels through the brain. Moreover, exercise and physical activity increase the number of connections between nerve cells thus ensuring a healthy brain. Exercise stimulates the brain thus keeping it healthy and less prone to degeneration. Scientists have also discovered that a healthy diet that is rich in vegetables reduces the rate of cognitive decline (Norton, & Brayne, 2014). Foods containing imega-3 fatty acids such as salmons and fish also reduce the occurrence of beta-amyloid plaques in the brain. Moreover, the engagement in mentally stimulating activities such as reading and engaging is sports activities reduce the risk of Alzheimer’s disease.

References

Jack, C. R., Knopman, D. S., Jagust, W. J., Petersen, R. C., Weiner, M. W., Aisen, P. S.,... & Lesnick, T. G. (2013). Tracking pathophysiological processes in Alzheimer's disease. The Lancet Neurology, 12(2), 207-216

Liu, M., Zhang, D., & Shen, D. (2014). Hierarchical fusion of features and classifier decisions for Alzheimer's disease diagnosis. Human brain mapping, 35(4), 1305-1319

Norton, S., Matthews, F. E., Barnes, D. E., Yaffe, K., & Brayne, C. (2014). Potential for primary prevention of Alzheimer's disease: an analysis of population-based data. The Lancet Neurology, 13(8), 788-794

Qiu, C., Kivipelto, M., & Strauss, E. (2009). Epidemiology of Alzheimer’s disease. Dialogues in Clinical Neuroscience, 11(2), 111–128

Selkoe, D. J., & Hardy, J. (2016). The amyloid hypothesis of Alzheimer's disease at 25 years. EMBO molecular medicine, 8(6), 595-608

Villemagne, V. L., & Ames, D. (2013). Amyloid? deposition, neurodegeneration, and cognitive decline in sporadic Alzheimer's disease: a prospective cohort study. The Lancet Neurology, 12(4), 357-367

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