The Chronic Neurological Disease Alzheimer s Disease

The Chronic Neurological Disease: Alzheimer’s Hollie Haywood South Piedmont Community College Abstract Alzheimer’s disease has been around since 1901; a German psychiatrist Alois Alzheimer was the first man to identify and follow a case that is now known as Alzheimer’s disease. Alzheimer’s disease is involved in synaptic deterioration and neuronal cell death, and causes degeneration in the hippocampus and amyloid deposition in blood vessels, ultimately cell death is the cause of the disease. There are various ways that someone can acquire the Alzheimer’s, a few include; family history, obesity, and Down syndrome. Some symptoms of the disease are, memory loss, difficulty completing familiar daily tasks, confusion with†¦show more content†¦In 1901, the German psychiatrist Alois Alzheimer studied a 51-year-old woman who experienced short-term memory, as well as a few other behavioral symptoms, until she died in April 1906 (Anderson). Within the past 15 to 20 years there have been dramatic discoveries made to help us understand the pathophysiology and neurogenetics of Alzheimer’s Disease, there are four different genes have been ultimately connected with this terrible disease as well as a few others that may be related (Anderson). According to Gould, in Alzheimer’s disease there is a constant a developing loss of intellectual function that will ultimately interfere with ones work, personal relationships, and their hygiene. With Alzheimer’s disease the brain becomes smaller and has narrower gyri and wider sulci, mainly in the frontal and temporal lobes (Gould, 2011, p. 522). Alzheimer’s disease affects three processes that keep neurons healthy: communication, metabolism, and repair. There are specific nerve cells in the brain which stop working and drop their connections with other nerve cells, and then they completely die (Anderson). The death or deterioration of the nerve cells is what impairs the memory in those who suffer with Alzheimer’s disease. The plaques, which disrupt the neura l conduction, contain fragments from beta-amyloid precursor protein; the role of