Amyloid Beta Peptide

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.

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.

Amyloid β-peptide (Aβ) is the major component of the senile plaques, and the amount of Aβ to form the plaques is correlative with the degree of neuronal damage and cognitive deficit. Although four million new cases of dementia are recognized yearly, and nearly 70% of these cases are ascribed to AD, there is still now not fully elucidated and no efficient method for its

Alzheimer 's disease (AD) is a progressive degenerative disease of the brain from which there is no recovery. There are three brain abnormalities that are the hallmarks of the Alzheimer’s disease is initially caused by plaques buildup in the brain’s neurons as illustrated in figure 1. The support structure that allows the flow of the nutrients through the neurons gets damaged and ultimately there is loss of connection among the neurons and they die off (National Institute of Health, 2015). This causes the brain tissue to shrinks, which is called atrophies. All this ultimately lead the victim of this disease to face difficulties in governing emotions, recognize errors and patterns, coordinate movement, and remember. Ultimately, a person with AD loses all memory and mental functioning.

It is a disease that we haven’t cured yet but instead have only come up and still coming up with treatment strategies to alleviate its symptoms. AD was first described in 1906 by a German psychiatrist by the name of Alois Alzheimer whilst he was performing a histophathologic study of his patient’s brain, a patient who had been suffering from dementia. His patient’s brain’s autopsy brought to light the presence of two types of lesions, which are senile plaques and neurofibrillary tangles. He saw a visible difference in the brain tissue for it was severely damaged by these lesions. Since then, our knowledge of AD’s cellular and molecular alterations has increased and we have come up with various hypotheses for AD that may soon help in developing effective preventative and therapeutic strategies. One of the most prevailing hypotheses that have already leaded to a number of therapeutic approaches is the amyloid cascade hypothesis. Hence, the following essay will explore the pathology of the amyloid cascade hypothesis and the evidence for and against it. It will also touch upon current progress in clinical trials that test the

In 1984 the criteria for diagnosing Alzheimer’s was developed by the Alzheimer’s Association. These three levels of diagnostic certainty were: Possible, Probable, and Definitive. In the Possible AD level, symptoms were not typical, but other disorders were ruled out. For example, it could be diagnosed if the patient had another illness, as well as with symptoms of dementia. The next level is Probable AD. In this level of criteria, the diagnostic evaluation excludes other causes of diagnostic decline. In addition to this, the historical pattern of functional and behavioral disturbances was noted. With these techniques, doctors were able to diagnose with an 85-95% accuracy. The last level was called Definitive AD. Within in this level, an autopsy was performed and the examined brain tissue revealed

A brain deteriorates, slowly being engulfed by a mysterious disease. The neurons being cut off and destroyed by two abnormal structures. First memory is affected gradually getting worse. Then one is unable to think properly, reason, and lacks of self control. Gaps are formed in the brain 's ventricles, due to the amount of dead tissue. In the end, it will lead to death. All of this may sound like something from a science fiction movie but infact its very real. These are all known possible symptoms of a common disease that affects about millions of Americans. It is known as Alzheimer 's disease (AD), and I plan on explaining it a bit more in this paper. First I will explain the disease and list some facts about it,then I will talk about some commonly asked questions about it.

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

Amyloid beta (Aβ) is a short peptide contains 37 to 43 amino acids and is well known for its hypothesized role in causing pathogenesis of AD, since one of the main hallmarks of AD is the accumulation of fibrillogenic Aβ in the grey matter of the brain (14-15). Meanwhile, over 90% of AD patients have cerebral amyloid angiopathy (CAA) which is characterized by the deposition of Aβ in capillaries, arteries, and arterioles (16-17). CAA causes the degeneration of smooth muscle cells and leads haemorrhages (17).

Alzheimer’s disease is a neurodegenerative of the brain that causes dementia, which is a loss in memory. Besides it being a neurodegenerative disease, many other conditions can cause dementia. Another kind of dementia is nutritional dementia, also called Wernicke-Korsakoff syndrome, or another which is alcohol syndrome, and it is caused by a lack of vitamin B1. Alzheimer’s disease usually appears in people over sixty-five years old. However, some cases of Alzheimer’s disease can happen at an early age of forty to fifty years old. This is called early-onset Alzheimer’s disease. It is caused by gene mutations that can be passed from parent to child. The most common form of late-onset Alzheimer’s disease is caused by the inability to clear amyloid-beta protein from the brain. Cerebrospinal is what help clear out the bad things in the brain, like amyloid-beta.

Brain specimens from people with AD tend to show varying amounts of cerebral atrophy associated with neuronal and synaptic loss. Such changes tend to occur over long periods of time and often begin long before noticeable

For people developing Alzheimer’s disease, there is no actual test to diagnose a person with it. Doctors will diagnose a person with Alzheimer’s disease when they have a severe cognitive decline that will meet the standards of dementia, dementia is very consistent that it will turn in to Alzheimer’s disease and that no other

Dementia is an umbrella term used to describe a group of diseases that may cause the brain to fail. The most common one is Alzheimer’s followed closely behind by Parkinson’s. Alzheimer’s was discovered in 1906 by Dr. Alois Alzheimer, who discovered changes in the brain of a woman who died of an unusual mental. Her symptoms included memory loss, language problems, and unpredictable behavior. Doctor’s now look at brain scans to see abnormal changes in the brain. Doctors may ask questions both to the patient and a family member of the patient, such as, over-all health, past medical problems, ability to carry out daily activities, and changes in behavior and personality. They also might conduct tests of memory, problem solving, attention, counting, and language

Emerging evidence demonstrates neuroinflammation as a crucial pathophysiology of AD, specifically impacted by microglia and astroglia. 3 The microglia are distributed evenly across the brain and are activated by protein aggregation and neuronal cell death. 3 Specifically related to AD, the two chief proteins involved are amyloid-B and tau.3 An accumulation of microglia around amyloid-B plaques has been documented in post-mortem human brains and in animal models with AD.3 Research has yet to clearly determine if microglial activation plays a beneficial or detrimental role in the progression of AD..3 Some reports suggest that microglia are attracted to

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