Abstract Every 67 seconds someone in the United States develops Alzheimer's disease (AD). AD is a neurodegenerative condition characterized by cognitive decline accompanied by memory loss. It is the only top ten cause of death in the United States which cannot be prevented, cured, or slowed. One of the proposed causes of AD is the formation of structures containing amyloid fibrils. Amyloid fibrils are insoluble fibrous protein aggregates sharing specific structural traits. Aside from AD, amyloid fibrils are associated with twenty other known human diseases, which arise from eighteen naturally occurring proteins or polypeptides which improperly fold to cause disease. Most of the current detection methods for AD are post-symptomatic. This means …show more content…
According to the Mayo Clinic, tangles are formed by interwoven tau proteins and plaques are formed by clusters of beta-amyloid proteins. Much research is focused on the beta-amyloid peptide, which forms amyloid fibrils and plaques. Amyloid fibrils are insoluble fibrous protein aggregates sharing specific structural traits. Aside from AD, amyloid fibrils are associated with over twenty other known human diseases, which arise from eighteen naturally occurring proteins or polypeptides which improperly fold to cause disease. The timeline of amyloid fibril formation consists of three distinct phases: the lag time phase, the elongation phase, and the asymptotic phase. During the lag time, proteins are beginning to form toxic species, but the concentration is difficult to measure. During the elongation phase, the detectable fibrils elongate exponentially. And finally, during the asymptotic phase, most of the available protein has been converted to amyloid fibrils; therefore, the growth discontinues, and the concentration remains …show more content…
Amyloid fibrils are toxic protein structures characterized by the presence of densely stacked β-sheets. Amyloid protein can arise from eighteen naturally occurring proteins or polypeptides which improperly fold to cause disease via a process called amyloidgenesis (Ramirez-Alvarado, 2000). These structures are extremely strong and appear to be immune to the effects of denaturing agents and proteases. The body’s inability to deconstruct these fibrous proteins leads to amyloidosis, or the abnormal accumulation of amyloid aggregates in the tissues of the body. The progression of this condition can lead to the manifestation of different pathogenic species, including the plaques and tangles which have long been associated with Alzheimer’s disease (Mayo Clinic,
structures called plaques. In Alzheimer's disease, similar plaques develop, but they are composed of fragments of a different protein.
Reports on the neurotoxic properties of Aluminum (Al++), as well as those of many other heavy metals, date as far back as the end of the nineteenth century. In 1965, Al was found to induce the formation of neurofibrillary tangles (NFT) in animal brains. These NFT’s were similar to those found in brains of patients suffering from Alzheimer’s Disease (AD). Vast research thus, was targeted at defining the possible etiologic role of Al in AD. However, several findings, among them the fact that Al++ induced NFT’s are structurally different than those found in AD, have contributed to reducing the importance placed on Al++ as an etiologic factor of AD. The Al++ theory, however, still remains a theory, and further research needs to be done before it can be disproved.
Clinically, Alzheimer’s disease is characterized by the accumulation of beta-amyloid plaque between living neurons in the brain (Sabbagh, 2008). This results in an excessive calcium influx inside the neurons and the breakdown of a protein called tau. Normally, the rol...
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.
Alzheimer’s disease or AD is an incurable disorder of the brain that results in loss of normal brain structure and function. In an AD brain, normal brain tissue is slowly replaced by structures called plaques and neurofibrillary tangles. The plaques represent a naturally occurring sticky protein called beta amyloid and in an Alzheimer’s brain, sufferer’s tend to accumulate too much of this protein. Neurofibrillary tangles represent collapsed tau proteins which, in a normal brain along with microtubules, form a skeleton that maintains the shape of the nerve cells. In Alzheimer’s disease, the tau proteins break loose from their normal location and form tangles. Without the support of these molecules, nerve cells collapse and die. As normal brain structure is lost with progression of the disease, brain function also degenerates. Patients afflicted with Alzheimer’s disease display a gradual mental decline. Initially, and most apparently, there is a loss of short-term memory. Eventually, as a patient progresses to later stages of the disease, the brain becomes so damaged that patients can no longer communicate or recognize immediate family or even themselves. They have difficulty walking and standing and frequently fall. In the final stages, they lose bladder and bowel control and have difficulty with swallowing, frequently leaving them malnourished and dehydrated. Eventually, they are forced to remain bedridden and, without the help of life-prolonging measures provided in a hospital, die. However, this level of deterioration is severe and may take as long as twenty years. Because of the disease’s slow progress and its usual later start in a person’s life, a victim of AD will usually die first of natural causes. Under the objectives ...
There are three different abnormalities that can make up Alzheimer’s disease. The first abnormality is beta-amyloid peptide cut from APP, a membrane precursor protein (Marieb and Hoehn 2013). Too much beta-amyloid is toxic and causes plaque buildup between neurons that reduces levels of acetylcholine which makes is difficult to retrieve old memories and make new ones (Marieb and Hoehn 2013). Another abnormality of Alzheimer’s disease is the presence of neurofibrillary tangles inside the neuron. These tangles consist of tau, a protein that leaves its stabilizing role and binds to another tau molecule forming a neurofibrillary tangle. (Marieb and Hoehn 2013). Neurofibrillary tangles then kill the neuron. The final abnormality of Alzheimer’s disease is brain shrinkage. The brain shrink...
Alzheimer’s disease comes from the last name of a neuro-psychiatrist from Germany, Alois Alzheimer. The disease was first diagnosed when a woman in her early fifties began experience memory problems. “Alzheimer recounted the now famous case of ‘Auguste D.’ a 51-year-old housewife who had been failing mentally for several years. As a result she had been admitted to his care in the Asylum for the Insane and Epileptic…” (Maurer and Maurer 1). After her death, he continued to examine her brain to find causes and explanations for her behavior. He discovered “…classic neuro-pathological signs of plaques and tangles” (Maurer and Maurer 1). “Plaques are chains of amino acids that are pieces of the amyloid precursor protein…tangles are aggregates of the protein tau” (Secko 1). As plaques develop they produce tangles and “these two abnormalities ultimately lead to loss of cognitive function” (Secko 1) Alois Alzheimer’s research has allowed many specialist to conclude that the apolipoproetein E gene may contribute to the disease.
This disease causes memory loss, difficulty in thinking processes, mood swings, depression, hallucinations, personality changes, and the inability to create new memories. Alzheimer’s disease is most common in people who are at the age of sixty years or older, but it can start as early as the age of nineteen. It can be categorized as a type of dementia. “Scientists believe Alzheimer’s disease prevents parts of a cell’s factory from running well” (Alzheimer’s Disease: The basics). Scientist believe that one cause of Alzheimer’s could be caused by plaques and tangles. Plaques are the build up of a protein called beta-amyloid in the nerve cells. Tangles are twisted fibers of the tau protein that build up inside of a cell. The exact cause of Alzheimer’s has not yet been determined, but scientists have reason to believe that it is because these plaques and tangles are blocking the communication of cells in the nervous system. Another probable cause is a mutation on the chromosomal genes 21, 14, and 1. This is why it is believed to be a genetically inherited
Alzheimer’s disease got its name from the German doctor, Dr. Alois Alzheimer. In 1906, he noticed that there were abnormal clumps and bundles of fibers i...
degeneration 3 A nerve cell has numerous axons and dendrites coming out of it. A neurofibrillary tangle is when the neuron changes. A number of dendrites are missing and the nucleus is filled with protein filaments resembling steel wool. Although all elderly people have a few of these helix shaped bundles in their brain as they are normal indicators of aging, Alzheimer's patients have. more than usual.
Alzheimer’s is a terrible disease, the diagnosis of which marks a long and painful journey through neurofibrillary degeneration. Unfortunately, there are so many factors that lead to and expedite the disease that synthesizing a cure is no simple task by any means. Whether the cause of the disease is hyperphosphorylation of tau or beta-amyloid plaques, current medical technology can only delay the symptoms. Hopefully the future of medical research will yield a method for reversing the progression of the neurological degeneration because far too many victims and their friends and family are forced to embark on the long and painful journey of Alzheimer’s.
Scientists believe that for most people, Alzheimer's results from a combination of genetics, lifestyle and environmental factors that affect the brain over time. Alzheimer's is caused by specific genetic changes that virtually guarantee a person will develop the disease. The causal effect for this disease is still unknown with fingers pointing to plaques and tangles in the brain. Although the causes of Alzheimer's are not yet fully understood, its effect on the brain is clear. Alzheimer's disease damages and kills brain cells. A brain affected by Alzheimer's disease has many fewer cells and many fewer connections among surviving cells than does a healthy brain. As more and more brain cells die, Alzheimer's leads to enormous brain shrinkage. When doctors examined an Alzheimer's brain tissue under the microscope, they saw two types of abnormalities that are considered the cause of the disease. One of these abnormalities is plaques that clump up, a protein called beta-amyloid which damages and destroys brain cells. In patients with Alzheimer’s the plaques created interfere with cell to cell communication. The other abnormality seen is tangles in the brain. Brain cells depend on an internal support and transport system to carry nutrients and other essential materials throughout their long extensions. This system requires the normal structure and functioning of a protein called tau. In an Alzheimer's patient, the threads of tau protein twist into abnormal tangles inside the brain cells, leading to failure of the transport system. (Alzheimer's Association) (National Institutes of Health, 2012)
In 1906, a German physician named Dr. Alois Alzheimer dealt with a patient that had been battling severe memory and confusion problems and had tremendous difficulty understanding questions and basic functions. Alzheimer suspected that the ailment had more to it than inherent memory loss. During an autopsy of the brain, he discovered that there were deposits of neuritic plaques surrounding the nerve cells and twisted fibers, known as neurofibrillary tangles, inside of the nerve cells. These observations became the definitive diagnosis of Alzheimer’s disease. The plaques and tangles that develop are a natural part of aging; however, they develop far more aggressively in Alzheimer’s victims. The plaques and tangles then block communication among nerve cells and disrupt the cells processes, eventually killing them. This destruction causes memory failure, personality changes, and problems carrying out everyday functions. Alzheimer’s especially attacks the memory. A victim in the later stage of the disease can...
Scientists know that Alzheimer disease is characterized by a gradual spread of sticky plaques and clumps of tangled fibers that disrupt the organization of nerve cells in the brain. However , a definite cause, prevention, or cause has not been found.
Alzheimer’s Disease is named after a German doctor, who specializes in the brain and nervous system, named Alois Alzheimer. This Disease forms in the brain. Alzheimer’s is the most common form of Dementia, a general term for memory loss and other intellectual abilities serious enough to enter. The Tau protein ensures the tubes in your brain stay straight allowing molecules to pass through freely. In Alzheimer’s Disease the protein collapses into strands or tangles, making the tubes disintegrate. There is visible differences of brain tissue in the from misfolded proteins called plaques and tangles. Beta-Amyloid clumps block signals and communication between cells in the brain. Researchers agree that Alzheimer’s Disease is m...