Week 10 assignment.pptx - Alzheimers Disease Walden University Advanced Pathophysiology NURS-6501N-25 Introduction Alzheimers disease(AD is the most

Week 10 assignment.pptx - Alzheimers Disease Walden...

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Alzheimer’s Disease Walden University Advanced Pathophysiology NURS-6501N -25 8/6/17
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. Alzheimer’s disease (AD) is the most common cause of dementia associated with a progressive neurodegenerative disorder. A prevalence of 44 million people throughout the world in 2015, and this figure is estimated to double by 2050 (Mendiola-Precoma et. al, 2016) Alzheimer’s disease (AD) is an age-related, progressive, and irreversible neurodegenerative disorder characterized by cognitive and memory impairment (Mendiola-Precoma et. al, 2016). Runs over 5-10 years, typically beginning with a learning impairment and recent memory loss. A frontal lobe gait imbalance appears. Steps are short, and shuffled, difficulty turning. High risk for falling backward (Hammer & McPhee, 2012). Later in the disease, social graces are lost. Paranoia, hallucinations, and delusions may occur. Terminal patients are bedridden, mute and incontinent (Hammer & McPhee, 2012) Introduction:
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Etiology: Unknown Amyloid PlaquesAmyloid plaques and neurofibrillary tangles are classic neuropathological signs of AD. Plaques mostly consist of protein fragment beta-amyloid which is produced by amyloid precursor protein (Alzheimer Association, 2017). Tangles consist of tau, a protein normally involved in maintaining nerve cells. Excessive phosphorylation appears to contribute to tangling and prevents protein from carrying out its normal function (Alzheimer Association, 2017). Cellular Damage:Damage to cellular structures by toxins or free radicals is also characterized with the pathology of AD. Brain inflammation is typical Alzheimer’s Association, 2017). Etiology: Unknown Amyloid PlaquesAmyloid plaques and neurofibrillary tangles are classic neuropathological signs of AD. Plaques mostly consist of protein fragment beta-amyloid which is produced by amyloid precursor protein (Alzheimer Association, 2017). Tangles consist of tau, a protein normally involved in maintaining nerve cells. Excessive phosphorylation appears to contribute to tangling and prevents protein from carrying out its normal function (Alzheimer Association, 2017). Cellular Damage:Damage to cellular structures by toxins or free radicals is also characterized with the pathology of AD. Brain inflammation is typical Alzheimer’s Association, 2017). Pathophysiology of Alzheimer’s Disease
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Genetic evidence links Amyloid B-peptide (AB) and B- amyloid precursor protein (APP) on chromosome 21q21.3- 22.05. About 10% of AD cases are familial, with early onset (before age 65) and autosomal dominant inheritance. About 70% of familial cases of AD are also linked to mutations in Presenilin 1 on chromosome 14q24.3. Another 14% have been associated with another gene, Presenilin 2 on chromosome 1q31-42 Huether & McCance, 2017).
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