Posted: July 17th, 2022

Alzheimer`s disease Critical Essay

Alzheimer’s disease is one of most prevalent medical conditions that affect the older sector of society. More and more people continue to suffer from this disease, but at present, there is still no cure available. So what causes Alzheimer’s disease? What are its effects, and are there any possible solutions for this condition? This essay would delve into the aforementioned details of Alzheimer’s disease. Before the nature of Alzheimer’s disease can be discussed, it is important to first define what dementia is.

This is because Alzheimer’s disease is identified as the most general cause behind the dementia not only in America but also throughout the world. Dementia refers to a syndrome which generally damages a person’s daily functioning. This is because the memory is impaired, as well as other thinking capabilities, such as reasoning and thought organization. Even the capacity for language and sight is also affected. Due to the memory decline, simple activities become difficult and patients need Helpance from others since they cannot take care of themselves anymore.

Consequently, Alzheimer’s disease is a medical condition which affects the brain; it is a disease that slowly develops, damaging one’s memory and other mental processes. These include “reasoning, planning, language, and perception. ” It is believed that the disease is caused by the overproduction or amassment of the protein called beta-amyloid; this protein is believed to result in the demise of nerve cells. The condition worsens as time goes by and can lead to death.
The possibility of acquiring Alzheimer’s disease increases as one ages, especially when one reaches the age of 70. Those who are beyond 85 years of age are most likely to be affected. However, it is important to point out that though memory loss is a normal part of aging, something as severe as Alzheimer’s disease is not part of it. Alzheimer’s disease was first discovered in 1906 by a German doctor named Alois Alzheimer; in 1910, the disease was officially named after him. Five years prior, Dr.
Alzheimer had 51-year-old patient named Frau Auguste D. ; the symptoms of her condition include problems of speech, memory and understanding. She even began doubting her husband’s loyalty for no reason at all. Her condition became worse and eventually, she died. When Dr. Alzheimer performed an autopsy, he found that the size of the brain had decreased. The most notable finding was that the cortex had significantly shrunk; the cortex is responsible for memory and speech, among other vital mental functions.
When her brain was viewed in the microscope, Dr. Alzheimer discovered brain cells which are either dead or in the process of dying. There were also fat and other deposits found in the blood vessels and brain cells. The brain is composed of neurons, which are nerve cells. These neurons produce signals which are chemical and electrical in nature. The signals are transferred from one neuron to another, enabling the person to think and recall. The transmission between neurons is made possible by neurotransmitters.
Those who suffer from Alzheimer’s disease experience the demise of neurons; eventually, neurotransmitters are also affected, and the brain functions are completely interrupted. The autopsy that Dr. Alzheimer performed on Auguste D. revealed that the brain tissues were characterized by “clumps” and “knots” of brain cells. At present, the former is recognized as plaques, while the latter is now identified as tangles. Both are acknowledged markers of Alzheimer’s disease. These two are also possible contributors in causing the brain disorder.
On one hand, plaques are composed of the aforementioned beta-amyloid protein. There is still no determined reason for the death of neurons, but the said protein is believed to be responsible for it. There are three genetic mutations that are recognized as responsible for a small percentage of the early-onset type of the disease. These three are as follows: “amyloid precursor protein, presenilin 1 protein (PS1) and presenilin 2 (PS2). ” The said mutations create plaques of amyloid. All three mutations are known to cause at least ten percent of all cases of Alzheimer’s disease.

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