How To Deal With Alzheimer's Disease

Alzheimer 's disease (AD) was discovered by a German doctor Alois Alzheimer in 1906 when he found amyloid plaques and neurofibrillary tangles in the autopsy of a woman who died of an unknown mental disease. The extracellular amyloid plaque deposits, composed of insoluble amyloid-Beta peptide were hypothesized to be the main etiological factor. “The most important abnormality is an excess of Amyloid-beta peptides brought about through either overproduction or failure in degradation.” (Uzun, Kozumplik, & Folnegović-Smalc, 2011) Later, it was discovered that intracellular neurofibrillary tangles composed of hyper-phosphorylated, helically-paired tau

1.1 Dementia is an umbrella term for a range of diseases that affect memory, behaviour and motor skills. The causes vary depending on the disease but largely the presence of “plaques” and “tangles” on the neurons of the brain is found in people with Alzheimer’s. Plaques are protein that the body no longer breaks down and allows to build up; these get between the neurons and disrupt the message transmission. Tangles destroy a vital cell transport system made of proteins. The transport system is organised in orderly parallel strands like rail tracks. In healthy areas a protein call “tau” helps the tracks stay straight but in areas where tangles

Alzheimer’s disease is a common problem in today’s society and within the older population this disease makes up the largest form of dementia. Although it is a problem in mainly older people, this disease can still occur in the younger population also. People in their 30s-50s can be diagnosed with this disease, even though it is not as common as people in their 60s-90s. The number of people with Alzheimer’s in the U.S. is close to five million and is expected to double within the next 30 years. With our modern medicine and advancements one would think a cure would be available, however, getting to the cause of the disease is a major factor. The cause of Alzheimer’s disease is one that is very debatable and questionable and most likely is a result of multiple factors rather than one. The main issue with finding the cause is because this disease affects the brain and can

Alzheimer's disease is one of the most common causes of dementia. The term 'dementia' describes a set of symptoms, which can include memory loss, changes in mood and problems with communication and reasoning. These symptoms occur when certain diseases and conditions, including Alzheimer’s disease, damage the brain. Alzheimer's disease could be described as a physical disease affecting the brain. During the course of the disease, protein 'plaques' and 'tangles' develop

Alzheimer’s disease is a complex illness that affects the brain tissue directly and undergoes gradual memory and behavioral changes which makes it difficult to diagnose. It is known to be the most common form of dementia and is irreversible. Over four million older Americans have Alzheimer’s, and that number is expected to triple in the next twenty years as more people live into their eighties and nineties. (Johnson, 1989). There is still no cure for Alzheimer’s but throughout the past few years a lot of progress has been made.

With the growing number of people becoming diagnosed, and experiencing symptoms of Alzheimer’s disease, we must begin to take precautions and somehow attempt to gain knowledge of how the disease can be better treated, and ultimately prevented.

Alzheimer’s: Scientists know that during Alzheimer’s two abnormal proteins build in the brain. They form clumps called either ‘plaques’ or ‘tangles’. These plaques and tangles interfere with how brain cells work and communicate with each other. The plaques are usually first seen in the area of the brain that makes new memories. A lot of research is focused on finding ways to stop these proteins in their tracks and protect brain cells from harm.

In the early stages of this disease Reagan stated; "I have begun the journey that will lead me into the sunset of my life." Research has been underway for years and years. One of the more promising avenues entertains the idea that these amyloid plaque proteins are the cause of changes in the brain. "The damage occurs when neurons congregate and form protein masses called amyloids that are water-soluble in normal brains but undergo structural changes and can't be dissolved in Alzheimer's patients. The masses disrupt nerve cell functions and begin to cause symptoms such as the loss of short-term memory. The deterioration of the brain is accompanied by a drop-off in the production of the neurotransmitter acetylcholine, which plays a key role in cognitive functioning" (p.444). I do believe that these amyloid plaques do play a role in the changes observed. These tangles and plaques are kind of the tell-tale sign that Alzheimer's is present. The missing piece to the puzzle is, What gets the ball rolling? What causes these changes to occur? I am confident that if we can find the answers to these questions, that we can find a cure.

Even today, after so much study, Alzheimer’s is not fully understood. However, researchers do agree that this degenerative disease is caused by the gradual buildup of fibrous protein compounds in the brain, which are known in the scientific world as amyloids. These amyloids in the brain area act like plaque and as a result of their presence, the normal brain functioning is disrupted.

The causes of Alzheimer’s are not yet fully understood; however, its effect on the brain can be understood. Alzheimer’s disease - insidious, attacking and terrifying - stalks and then murders brain cells. A brain afflicted with Alzheimer’s disease has a decreased count in cells and connections among cells. The more brain cells die, the smaller the brain of a person with Alzheimer’s gets. When doctors examine a brain with Alzheimer’s tissue, they see two types of deformities that are known to be trademarks of the disease. The first trademark is known as plaque, which is a cluster of a beta-amyloid protein that may damage and kill brain cells in a number of ways, including blocking with cell-to-cell communication. Whereas the final cause of brain-cell death in Alzheimer’s remains a mystery, the groups of beta-amyloids that cover the brain cells are a sure sign of the disease. The second trademark of Alzheimer’s is the tangle. Brain cells are reliant on internal support and a transport system to bring nutrients and other essentials to their distant regions. This system needs a protein called tau. In Alzheimer’s, strings of tau protein roll into abnormal tangles inside brain cells, concluding in failure of the cell's transport system. This breakdown of the system is powerfully involved in the decline and death of brain

Damage or lesions to the brain are the main causes of Alzheimer’s disease; the two main causes of these lesions are neurofibrillary tangles and senile plaques. (4) These are commonly known as plaques and tangles and are caused by the build-up of two proteins. The plaques are a build-up of the protein beta-amyloid (β-amyloid) while the tangles are formed by the build-up of the protein tau, even though both are found in Alzheimer's disease only the β-amyloid plaques are unique to the disease and it is these plaques that are believed to be the primary cause of Alzheimer's.

Someday it may be possible to deal with people at risk for Alzheimer's disease by keeping tau low. Consider how taking drugs that reduced cholesterol has enabled control the accumulation of cholesterol in blood vessels that results in atherosclerosis and also heart

The two main biomarkers of AD are beta-amyloid (Aβ) and tau and are highly debated in regards to their function in AD pathophysiology. The production of beta-amyloid plaques may be due to improper functioning of the proteasome preventing the breakdown of Aβ. Support for this theory comes from research indicating that the 20S proteasome is responsible for Aβ degradation and that alterations to the kinetics of the proteasome increased Aβ levels (Zhao & Yang, 2010). These accumulated levels of Aβ plaques leads to lower levels of soluble Aβ, which is needed for memory formation. This may occur through activation of nicotinic acetylcholine (ACh) receptors and AChE levels are drastically reduced in AD patients. (Garcia-Osta & Alberini, 2009). The microtubule stabilizing protein tau may become hyper-phosphorylated in AD due to the presence of high levels of Aβ. Hoshi et al (1996) showed that Aβ exposure to rat hippocampal neurons in vitro produced increased levels of the tau kinase GSK-3 (glycogen synthase kinase 3) which in turn hyper-phosphorylated tau leading to cellular death. (Hoshi et al., 1996) The neurotoxicity of tau may not be produced solely because of GSK-3, but may be due to

There is a large supply of amyloid plaques in the cells of people with Alzheimer’s disease. Amyloid plaques are clustered pieces of protein that build up between nerve cells. They speed up the production of beta amyloid, which are polypeptides of about thirty-six to forty-three amino acids long (emedicinehealth, 2014; Stanford Medicine, 2013). Amyloid precursor proteins (APP), when split into specific pieces, are producers of beta amyloid. They are found in tissues and organs, such as the brain. Amyloid precursor proteins pass through a fatty membrane on the outside of a cell. This allows them to extend from the

Alzheimer's Disease is a condition that affects 50% of the population over the age of eighty five, which equals four million Americans each year. It is becoming an important and high-profile issue in today's society for everyone. There are rapid advancements being made in the fight against this disease now more than ever, and the purpose of this essay is to educate the public on the background as well as the new discoveries. There are many new drugs that are being tested and studied every day which slow down, and may even halt the progress of the disease.