Alzheimer's Disease Essay

1. Introduction

Alzheimer’s disease is a neurodegenerative disorder that is on the rise among ageing populations worldwide. Alzheimer’s disease leads to the death of neurons in numerous areas of the brain, including the hippocampus and cerebral cortex, which are two areas of the brain correlated with memory. (5) According to the Alzheimer’s Association, the number of people diagnosed with Alzheimer’s disease could rise from 5 million to 16 million in the United States and by 2050 the total worldwide is predicted to rise to 100 million. This could relentlessly strain health-care systems because the

Disease is so persistent, disabling, and costly. Based on postmortem examinations of remaining brain tissues in Alzheimer’s patients, Amyloid plaques, and neurofibrillary tangles are the two main characteristics involved with Alzheimer’s disease. (5) Amyloid-B is a protein that accumulates on the inside and outside of neurons. High levels of amyloid proteins damage axons and dendrites. (3) These damaged axons and dendrites cluster into structures called amyloid plaques, which begin to form before any behavioral symptoms appear (3). As the plaques accumulate, the cerebral cortex, hippocampus, and other areas atrophy or waste away (3). In addition to amyloid-B, these neurofibrillary tangles accumulate from tau proteins (3). Tau proteins are the intracellular support structure for neurons. Tau proteins help assemble and maintain microtubules that transport nutrients along axons (5). However, in Alzheimer’s disease, tau undergoes changes that cause it to bind to itself, resulting in neurofibrillary tangles (5). Therefore, the combination of amyloid and tau produces the behavioral deficits seen in those who suffer from Alzheimer’s disease ...

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...a continuous flow of ATP. In order to support a constant flow of ATP, the mitochondria are concentrated at synapses. If these changes in the organelle functions continue in an altered state, there is a greater risk of affecting the synaptic plasticity. In addition, the “paucity of mitochondria causes the synaptic dysfunction in dendrites and axons” (2). Therefore, synaptic mitochondrial dysfunction is indicative of Alzheimer’s pathogenesis (2).

Additional experiments could be performed in order to enhance the relevance and accuracy of the current study. According to the authors, it is necessary to “reveal how the NH2 20-22 kDa tau fragment targets AD mitochondria and if and how it actually impairs the mitochondrial physiology” (2). I would also be interested in researching how nutrition and lifestyle play a role in treatment and prevention of Alzheimer’s disease.