All About Alzheimer’s Disease

Author: Camille Jessica Cunanan


Alzheimer’s Disease is a brain disorder that gets worse as it progresses and affects 15 million people throughout the world. The number of people who are predicted to develop Alzheimer’s Disease in the United States is projected to grow to about 13.8 million people by the mid-century. Individuals who suffer from Alzheimer’s Disease experience dementia, which is characterized by memory loss, personality changes, and impaired reasoning. There are two forms of the disease – Sporadic and Familial Alzheimer’s Disease. Sporadic Alzheimer’s Disease is the most common form and is late-onset, meaning it occurs in older people who are around 80 years old. On the other hand, familial Alzheimer’s Disease is less common and it can be inherited from family members. Familial Alzheimer’s Disease is considered early-onset, meaning it occurs in younger people who are around 45 years old.


There are many believed reasons why Alzheimer’s Disease starts. Some research has pointed towards amyloid-β. Amyloid-β is a type of protein and when it is mutated or genetically changed, it can bind with other amyloid-β proteins and form clumps or plaques. These plaques can then travel throughout the body and embed themselves in brain cells, which are called neurons. Eventually, when there are too many plaques in the neurons, it gets damaged, which is what causes the memory loss. Some research has shown that amyloid-β clumps form because of a dysfunction in the amyloid-β precursor protein, which is often abbreviated APP. APP contains a piece of amyloid-β. Amyloid-β then gets cut off by enzymes called β‑secretases or γ‑secretases  and then gets released from the cell and travels throughout the body. When this function does not happen normally, like in the state of Alzheimer’s Disease, amyloid-β does not get broken down and can ultimately aggregate into plaques.


In addition to amyloid-β, tau proteins have been correlated to the progression of Alzheimer’s Disease. Tau proteins are microtubule-associated proteins, which are involved with maintaining the structure and strength of a cell. Mutations in the genes of tau proteins causes them to bundle up and form “tau tangles” or “neurofibrillary tangles” in brain cells. This then causes neurological damage and impaired brain function. Many tau tangles are found in the brains of patients with Alzheimer’s Disease, which is why tau proteins have been strongly correlated to the development of the disease.


While some scientists and doctors believe that the effects of amyloid-β and tau proteins are separable and independent of each other, some research has led them to believe that both amyloid-β and tau proteins work together and cooperatively cause Alzheimer’s Disease. According to a recent study, lifestyle choices such as a lack of sleep and psychological stress can disrupt amyloid-β levels and encourage the formation of plaques. The formation of amyloid-β plaques is characterized as the preliminary symptom of Alzheimer’s Disease. As years go on and as the disease progresses, the increase in amyloid-β plaques encourages the formation of tau tangles. This formation of tau tangles causes the disease to get worse and intensify memory loss and brain dysfunction.


Diagnosing Alzheimer’s Disease has been difficult for physicians because different people exhibit different symptoms. For some people, the signs of the disease are more or less obvious than others, causing many misdiagnoses. However, with the rapid development of tools and techniques for imaging human brains, doctors and scientists can better understand how the brain works and further study brains with Alzheimer’s Disease. For example, MRIs which stands for magnetic resonance imaging, and PET scans, which stands for positron emission tomography, have helped doctors look at brains and detect the symptoms of the disease. PET scans and MRIs allow doctors to measure how much amyloid-β or tau proteins have accumulated in the diseased brain.


The treatment of Alzheimer’s Disease can involve non-pharmacological and pharmacological methods. Non-pharmacological methods involves the treatment of the disease without the use of drugs and medication. Instead, doctors have practiced exercising the mental abilities of patients with Alzheimer’s disease. Non-pharmacological treatments include memory training, verbal fluency, and verbal learning. However, even though non-pharmacological treatments have shown to have a positive effect on reversing or preventing memory loss, there is not much evidence for the long-term maintenance and improvement on the effects of brain function of individuals suffering from the disease.


Conversely, treatment of the disease using pharmacological methods involves treating patients with medication. Because symptoms of the disease are very different among patients, trying to find the best and most appropriate drug for the patient has proven to be difficult. As a result, doctors have focused their drug treatments on maintenance of comfort rather than trying to cure the disease.

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