D027 phase 3 portfolio

Feedback and Synthesis Improvement Plans I met with an ARNP that I have been working with for several years, her name is K. Sherrouse. I received positive feedback from her. I was considering doing my synthesis on Cancer but after speaking with K.S. I chose Alzheimer's Disease. Both are incredibly debilitating illnesses however, we recently had a friend die from Cancer so that was there were too many emotions at the time. Other feedback I received was I had not gathered enough information so after speaking with K.S. I researched more. According to K.S. my synthesis was approved. The plan will be to start the synthesis with the statistics on Alzheimer's Disease. Pathophysiology Synthesis Alzheimer’s disease (AD) is the sixth-leading reason of fatality and is 70% present in all cases of dementia. The global burden of AD is expected to accelerate from 26.6 million cases in 2006 to 106.8 million by 2050 ("About Healthy People | Healthy People 2020", 2020). AD is generally regarded as disorders related to strengthen the loss of neurons and synapses proceeds in distinct anatomical loci, resulting in different phenotypes. The pathophysiology of Alzheimer's disease is attributed to several factors such as the cholinergic dysfunction, amyloid/tau toxicity and oxidative stress/mitochondrial dysfunction. Some of the pertinent points include the pathophysiology, clinical manifestations, and diagnostic methods. The pathophysiology of AD are neuronal loss and/or pathology may be seen particularly in the hippocampus, amygdala, entorhinal cortex and the cortical association areas of the frontal, temporal and parietal cortices, but also with subcortical nuclei such as the serotonergic dorsal raphe, noradrenergic locus coeruleus, and the cholinergic basal nucleus. The deposition of tangles follows a defined pattern, starting from the trans-entorhinal cortex; consequently, the entorhinal cortex, the CA1 region of the hippocampus and then the cortical association areas, where frontal, parietal and temporal lobes are particularly affected. The extent and placement of tangle formation correlates well with the severity of dementia, much more so than numbers of amyloid plaques. Considerable amount of the cognitive dysfunction in AD is not due to loss of one neurotransmitter but rather to disruption of network connections between several key brain regions within the limbic system and specific areas of the neocortex. Clinical manifestations of AD are typically a disease of older age. It is exceptional for AD to occur before age 60. The rate and prevalence of AD grow exponentially with age, essentially doubling in prevalence every 5 years after the age of 65 years (Alzheimer’s Association, 2015)