Saturday, August 10, 2019

Pathophysiology of Late Onset Alzheimer's Disease Research Paper

Pathophysiology of Late Onset Alzheimer's Disease - Research Paper Example Alzheimer’s is normally classified into three different groups; Early onset, Late onset and familial. This paper analyses the dimensions of late onset Alzheimer’s. Pathophysiology of "Late Onset" Alzheimer's Disease It is estimated that more than 4.5 million people in America alone experiencing Alzheimer’s currently. Doraiswamy et al, (2009) have mentioned that Alzheimer’s can occur even at the age of forties or fifties (Doraiswamy et al, 2009, xvii). However, about 90% of the Alzheimer’s disease patients are victims of "Late Onset" Alzheimer's. Alzheimer's victims of more than 65 years of age are normally included in the category of Late Onset" Alzheimer's. Only 10% of Alzheimer's victims are below the age of 65. Normally people below the age of 65 suffers Alzheimer’s because of Down syndrome. This type of Alzheimer’s is known as Early onset Alzheimer’s. On the other hand, "Late Onset" Alzheimer's disease is caused by hereditar y and environmental factors. A third type of Alzheimer’s is known as Familial Alzheimer's disease (FAD). In the case of FAD patients, the disease is caused by family history or hereditary. ... It has the ability to recollect everything in the distant memory while facing problems in recollecting information stored in the recent memory. Bonda et al. (2010) pointed out the imbalances between mitochondrial fission and fusion of cell proliferation as the reason for Alzheimer’s. â€Å"Specifically, the dynamic balance of fission and fusion in AD is greatly shifted toward fission, and, as a result, affected neurons contain abnormal mitochondria that are unable to meet the metabolic demands of the cell†(p.181). It should be noted that fission is the process of breaking of cells whereas fusion is the process of combining cells. Both fission and fusion are necessary body mechanisms to maintain good memory. However, in the case of patients with Alzheimer’s fission mechanism occurs more while fusion mechanism occurs less. As a result of that cell proliferation procedures will be troubled and the communication though neurons become defective. It should be noted tha t neurons are responsible for sending instructions from the brain to different parts of body. This communication process may become defective because of the imbalances in fusion and fission. Risk Factors Advanced age is the primary risk factor for AD; risk doubles every 5 years after the age of 65. Additional risk factors include having a first-degree relative with AD; Down syndrome; head trauma; certain environmental exposures, including metals, infection, and toxins; decreased estrogen levels; and mutations in the APP, PSEN1, PSEN2, or APOE genes. Cardiovascular disease, cardiovascular risk factors (e.g., hypertension, obesity, dyslipidemia, insulin resistance), depression, and certain lifestyle choices (e.g.,

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