1. Introduction
Alzheimer’s disease can be characterized as a neurodegenerative disease where an individual suffers from progressive loss of memory and basic mental functions. Because researchers cannot pinpoint a specific factor that causes Alzheimer’s disease, many theories exist regarding its causation. One such theory, the dysfunction mitochondria within an individual’s brain cells, the organelle’s DNA mutation, and the implications these two variables have on the causation of Alzheimer’s disease is a leading theory among the scientific community and is therefore explored. A second and more controversial theory, aluminum exposure as a risk factor and eventual development of Alzheimer’s disease is also considered. the former theory is shown …show more content…
Such factors include age, environment, lifestyle choices, nutrition and diet, and genetics. However, the presence of these risk factors do not, by themselves, guarantee an individual’s development of Alzheimer’s disease. Before laying out their argument that abnormal mitochondrial function in the brain may be a cause of Alzheimer’s disease, Reddy & Beal were careful to first distinguish the causal differences between early and late onset Alzheimer’s disease. Reddy and Beal argued that an individual’s genetic make-up is crucial in the causation of early-onset Alzheimer’s disease, a form of Alzheimer’s that is inherited through family genes. However, they also point out that this form of Alzheimer’s disease is rare and only accounts for two to three percent of individuals suffering from the disease. Therefore, Reddy and Beal focused mainly on explaining the possible causation of late-onset Alzheimer’s disease by arguing that the disease may be caused by mitochondrial abnormalities in the …show more content…
The first of three arguments that Munoz points to is aluminum toxicity. While Munoz did not dispute that extreme levels of aluminum exposure to the human body is not toxic. Munoz however, argued that immunohistochemistry, a method used to determine the protein make-up of a given sample (aluminum), showed that aluminum tangles where made out of normal neurofilaments compared to the immunohistochemistry of Alzheimer’s disease’s related tangles, neurofibrillary, which are made up of tau proteins. Additionally, Munoz found that any symptoms of syndromes or diseases experienced by individuals due to high levels of aluminum exposure, are not similar symptoms that a traditional induvial with Alzheimer’s disease would experience. Lastly, Munoz argued that, while aluminum is a toxin, so are many other elements that the human body consumes. Therefore, the routes that Alzheimer’s disease takes in manifesting itself does not in any way resemble the route aluminum takes in affecting the body and
Alzheimer’s disease can be characterized as a neurodegenerative disease where an individual suffers from progressive loss of memory and basic mental functions. Because researchers cannot pinpoint a specific factor that causes Alzheimer’s disease, many theories exist regarding its causation. One such theory, the dysfunction mitochondria within an individual’s brain cells, the organelle’s DNA mutation, and the implications these two variables have on the causation of Alzheimer’s disease is a leading theory among the scientific community and is therefore explored. A second and more controversial theory, aluminum exposure as a risk factor and eventual development of Alzheimer’s disease is also considered. the former theory is shown …show more content…
Such factors include age, environment, lifestyle choices, nutrition and diet, and genetics. However, the presence of these risk factors do not, by themselves, guarantee an individual’s development of Alzheimer’s disease. Before laying out their argument that abnormal mitochondrial function in the brain may be a cause of Alzheimer’s disease, Reddy & Beal were careful to first distinguish the causal differences between early and late onset Alzheimer’s disease. Reddy and Beal argued that an individual’s genetic make-up is crucial in the causation of early-onset Alzheimer’s disease, a form of Alzheimer’s that is inherited through family genes. However, they also point out that this form of Alzheimer’s disease is rare and only accounts for two to three percent of individuals suffering from the disease. Therefore, Reddy and Beal focused mainly on explaining the possible causation of late-onset Alzheimer’s disease by arguing that the disease may be caused by mitochondrial abnormalities in the …show more content…
The first of three arguments that Munoz points to is aluminum toxicity. While Munoz did not dispute that extreme levels of aluminum exposure to the human body is not toxic. Munoz however, argued that immunohistochemistry, a method used to determine the protein make-up of a given sample (aluminum), showed that aluminum tangles where made out of normal neurofilaments compared to the immunohistochemistry of Alzheimer’s disease’s related tangles, neurofibrillary, which are made up of tau proteins. Additionally, Munoz found that any symptoms of syndromes or diseases experienced by individuals due to high levels of aluminum exposure, are not similar symptoms that a traditional induvial with Alzheimer’s disease would experience. Lastly, Munoz argued that, while aluminum is a toxin, so are many other elements that the human body consumes. Therefore, the routes that Alzheimer’s disease takes in manifesting itself does not in any way resemble the route aluminum takes in affecting the body and