Pathophysiology of Late Onset Alzheimer's Disease Research Paper

Pathophysiology of Late Onset Alzheimers Disease - Research Paper ExampleAlzheimers is normally classified into three different groups Early onset, Late onset and familial. This paper analyses the dimensions of late onset Alzheimers. Pathophysiology of Late Onset Alzheimers Disease It is estimated that more than 4.5 jillion people in America alone experiencing Alzheimers currently. Doraiswamy et al, (2009) have mentioned that Alzheimers can occur even at the age of forties or mid-fifties (Doraiswamy et al, 2009, xvii). However, about 90% of the Alzheimers disease patients be victims of Late Onset Alzheimers. Alzheimers victims of more than 65 years of age are normally included in the category of Late Onset Alzheimers. Only 10% of Alzheimers victims are below the age of 65. Normally people below the age of 65 suffers Alzheimers because of tear down syndrome. This type of Alzheimers is known as Early onset Alzheimers. On the other hand, Late Onset Alzheimers disease is caused by her editary and environmental factors. A third type of Alzheimers is known as Familial Alzheimers disease (FAD). In the case of FAD patients, the disease is caused by family history or hereditary. ... It has the superpower 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 uniting of cellular telephone proliferation as the reason for Alzheimers. 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 Alzheimers fission mechanism occ urs 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 that 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 jeopardy 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.,