The Relationship Between Beta-Amyloid and Tau and Their Reease affects over 40 million people in the world. It is a costly disease that robs the afflicted person of their mental capacity over a period of five to twenty years. In the United States alone, there are five and a half million people that have the disease (Alzheimer’s Association).
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Alzheimer’s Disease is also the only disease in the top ten leading causes of death in people over the age of 65 that cannot be cured, prevented, or slowed. What are researchers doing to try to prevent this disease? Researchers are currently taking steps by trying to figure out how beta-amyloid and tau relate to each other and how these two proteins play a role in Alzheimer’s Disease.
Millions upon millions of dollars of research and hours have been spent in researching how to prevent this disease. Alzheimer’s Disease is currently the only disease in the top leading causes of death of people above the age of 65 that cannot currently be prevented, slowed, or cured. This presents a great challenge to researchers that want to help people afflicted with Alzheimer’s Disease and other types of mental degenerative diseases. To do that researchers must find out what causes Alzheimer’s Disease and what it is characterized by.
Alzheimer’s Disease is currently a Subtype of Dementia. To understand it better, researchers must be able to understand what dementia is and the different stages that are included throughout the progression of the disease. Dementia is characterized by the continued loss of memory and mental function until the afflicted can no longer perform household tasks such as bathing and going to the bathroom. According to the Mayo Clinic, there are five different stages of Alzheimer’s Disease and these include: Preclinical Alzheimer’s Disease, MCI (Mild Cognitive Impairment), Mild Dementia, Moderate Dementia, and Severe Dementia (Mayo Clinic).
Preclinical Alzheimer’s Disease is the first stage in this disease. Preclinical Alzheimer’s Disease takes place years before any noticeable symptoms can be observed. There are many changes going on in the brain during this period. There are noticeable signs in the brain’s structure but a person does not show a cognitive decline. The people around someone with Preclinical Alzheimer’s Disease will not be able to notice anything different about the person that has it. Neither will the person afflicted. This stage is often the longest stage of the disease because the onset is very gradual and can take decades to progress to the next stage of the disease. This stage also goes undetected because you would need to have tests that show the brain with a baseline and follow up tests for comparison.
The second stage of Alzheimer’s Disease is Mild Cognitive impairment or MCI. MCI has little effect on work and social life. People with MCI may tend to have memory lapses or difficult remembering the steps of how to do something. This stage usually lasts about two years before it advances into the next stage of Alzheimer’s Disease. It is also important to note that people with MCI do not always have Alzheimer’s Disease but that people with Alzheimer’s disease will go through the MCI stage of the disease.
The next stage in Alzheimer’s Disease is mild dementia. People with Alzheimer’s are mostly diagnosed with the disease in this stage because of the significant increase in trouble with cognitive tasks. Individuals in this stage will often ask the same question multiple times because they cannot remember the answer to it as well as having difficulty solving complex problems. They may also have difficulty expressing thoughts and expressing themselves, and possibly go though personality changes. These personality changes are different based on the person, but one may be more irritable or become more withdrawn in social situations.
Moderate dementia is the next stage in Alzheimer’s Disease. Individuals in this stage should no longer be left to care for themselves because of their cognitive decline. They show increasingly poor judgement and have trouble making good decisions. They also experience an even greater loss of memory and more major personality changes. Individuals may mistake family members and friends as the same person and strangers as family members. It is not uncommon for individuals in this stage of Alzheimer’s Disease to think that people are stealing from them or see and hear things that are not there. People may forget to do daily activities such as eating and drinking or may not be able to find the bathroom and should no longer be left to live on their own.
Severe dementia is the last stage in Alzheimer’s Disease. It can also be called advanced dementia or late stage dementia. During this stage one’s ability to do daily tasks is no longer there and they need a full time caregiver. Commonly one will also lose the ability to speak coherently and can no longer communicate what they want or need to their caregiver. Many people do not make it to this stage of the disease but those that do are expected to live one to three years.
Alzheimer’s Disease can last for up to twenty years but most that are diagnosed with the disease only live about six to twelve years after the diagnosis. The factors in how long someone that has will live are various. There are genetic factors that can speed up or slow down the process as well as simple things such as diet and activity level.
There are many different factors that go into developing Alzheimer’s Disease, but researchers agree that there are two proteins in the brain that are mostly to blame. According to the World Alzheimer’s report 2018, One is called beta-amyloid, usually just called amyloid the other is called tau (Patterson, 8). These two proteins reach levels both reach abnormally high levels are start to prevent cognitive function. Scientists currently do not know why these proteins rise to these abnormally high levels or what relationship they have to each other. To try to understand more about how to prevent and cure the disease scientists must look at what each of these proteins do to the brain.
Amyloid is a fragment of the amyloid precursor protein. According to PDB-101: Acetylcholine Receptor, It [the amyloid precursor protein] is a large membrane protein that normally plays an essential role in neural growth and repair. However, later in life, a corrupted form can destroy nerve cells, leading to the loss of thought and memory in Alzheimer’s disease (PDB-101: Acetylcholine Receptor). This protein is a very important part of neural growth and for that reason, researchers say that they cannot simply just shut off the production of this protein. So what happens next?
The problem isn’t with the amyloid precursor protein (APP) but with what it leaves behind after it has been used. What is left behind is commonly called beta-amyloid. In younger people, this toxic fragment is recycled by the body and cannot harm the brain cells. In individuals with Alzheimer’s Disease, the protein is not broken down fast enough which results in the toxic fragments of APP bonding together and forming a plaque. This buildup causes two different things to happen because of the properties it possesses.
The properties that the built up amyloid has is that it is toxic to the brain cells, and the plaques also restrict any possible growth in the brain. Amyloid also causes mutations in different cells and proteins in the brain. This causes a mutation in tau which is the other protein in the brain that is a major factor in why the tau protein starts to become toxic to the brain.
Tau is a protein in the brain that helps build the structure of the brain itself. According to Eva-Maria Mandelkow and Eckhard Mandelkow, Tau was one of the first microtubule-associated proteins (MAPs) to be characterized(Mandelkow, E.-M., and E. Mandelkow). Microtubules are structures that help transport materials used in cells be transported as well as helping provide the so called scaffolding of the brain. Tau helps bind these microtubules to the cells and to each other(Hyman et al.). Unlike other proteins, tau does not fold itself and is a very long molecule in the body. According to Eva-Maria Mandelkow and Eckhard Mandelkow, Tau is normally a cytosolic protein, but its occurrence outside cells has become important for studying and diagnosing the Alzheimer’s Disease disease process(Mandelkow, E.-M., and E. Mandelkow). Since tau can be found outside of cells, it builds up in the the cerebrospinal fluid (CSF) at an early stage of Alzheimer’s Disease and therefore serves as a biomarker (Mandelkow, E.-M., and E. Mandelkow).
Tau is also a very important protein to the brain and the rest of the body which is why researchers must try to find another way to prevent it from mutating and becoming toxic to the brain instead of just trying to limit the amount the the body can produce like they can with other proteins that play a less important role. When this protein mutates it starts to bond to itself instead of other cells that it normally bonds to. Because this protein can be outside of the cells in the brain, it can form clumps called neurofibrillary tangles. According to the Bright Focus Foundation, Neurofibrillary tangles are insoluble twisted fibers found inside the brain’s cells. These tangles consist primarily of a protein called tau, which forms part of a structure called a microtubule (Bright Focus Foundation). This causes the protein to become toxic to the brain itself even though it is an essential protein in the body. It starts to cause the brain calls to shrink and die. It also starts to block neural pathways as well which is what causes the majority of memory loss in Alzheimer patients.
So how do these two proteins relate to each other? When amyloid is not broken down it starts to build plaques that restrict brain growth and causes mutations. One of these mutations happens to the tau protein in the brain which plays an important role in creating the brain structure. When this protein mutates, it rises to abnormal levels and starts to bond to itself. This then allows for tau protein clumps called neurofibrillary tangles to to become toxic to the brain tissue and also block neural pathways.
There is also another factor that these two proteins have on the brain. When these two molecules reach abnormal levels, they start to interact with each other. Amyloid starts to encase the tau protein clumps. When this happens they create another toxic element to the brain. When these two molecules interact they also amplify the toxic effects that each one has on the brain resulting with a compounding effect.
Interestingly enough, according to Small and Duff, mutations in both genes encoding APP and tau were found to cause dementing illness(Small, Scott A., and Karen Duff). Since amyloid plaques also cause more mutations in the genes of cells, it can cause this same mutation that causes tau to form neurofibrillary tangles inside of neurons.
Scientists have come up with a way to possibly cure Alzheimer’s Disease. When the amyloid protein starts reaching abnormal levels, there is a short period of time during the preclinical phase of Alzheimer’s Disease that a amyloid reducing pharmacological agent can be introduced into the brain. According to small and duff, a pharmacological agent that reduces brain A?? levels should act as an effective drug against the disease (Small and Duff). This is a very promis
In total, Alzheimer’s Disease is a very devastating disease that is very complicated. Tau and beta-amyloid play big roles in causing each other to rise to abnormal level and both play a big role in causing Alzheimer’s Disease. Only in recent years, researchers have just found out what causes the brain to decline in cognitive function at such a significant rate. There are five stages going from no symptoms at all to completely robbing someone of their ability to live on their own and make choices for themselves. Two major proteins that are responsible for causing AD are beta-amyloid and tau. Each of these toxic factors to the brain come from things that play a major role in brain structure and development. There are some things that scientists can do to attempt to slow down the progression of the diseaseand maybe even cure it but is ineffeective due to the fact that by the time one knows they have AD, the disease has already started a wildfire that is breaking down their brain and scientists do not know how to stop this from happening in the brain.
Amyloid Plaques and Neurofibrillary Tangles. BrightFocus Foundation, 28 Nov. 2018, www.brightfocus.org/alzheimers-disease/infographic/amyloid-plaques-and-neurofibrillary-tangles.
Mandelkow, E.-M., and E. Mandelkow. Biochemistry and Cell Biology of Tau Protein in Neurofibrillary Degeneration. Cold Spring Harbor Perspectives in Medicine, vol. 2, no. 7, 2012, doi:10.1101/cshperspect.a006247.
PDB101: Molecule of the Month: Amyloid-Beta Precursor Protein. PDB-101: Acetylcholine Receptor, pdb101.rcsb.org/motm/79.
Rajmohan, Ravi, and P. Hemachandra Reddy. Amyloid-Beta and Phosphorylated Tau Accumulations Cause Abnormalities at Synapses of Alzheimer’s Disease Neurons. Journal of Alzheimer’s Disease, vol. 57, no. 4, 2017, pp. 975“999., doi:10.3233/jad-160612.
Small, Scott A., and Karen Duff. Linking A?? and Tau in Late-Onset Alzheimer’s Disease: A Dual Pathway Hypothesis. Neuron, vol. 60, no. 4, 2008, pp. 534“542., doi:10.1016/j.neuron.2008.11.007.
Spires-Jones, Tara L., and Bradley T. Hyman. The Intersection of Amyloid Beta and Tau at Synapses in Alzheimer’s Disease. Neuron, vol. 82, no. 4, 2014, pp. 756“771., doi:10.1016/j.neuron.2014.05.004.
Stages of Alzheimer’s. Alzheimer’s Association, Alzheimer’s Association, www.alz.org/alzheimers-dementia/stages.
Wortmann, Marc. World Alzheimer Report 2014: Dementia and Risk Reduction. Alzheimer’s & Dementia, vol. 11, no. 7, 2015, doi:10.1016/j.jalz.2015.06.1858.
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