Characterized by the symptoms it presents, most noticeably a decline in cognitive function, Alzheimer’s Disease is a neurodegenerative disorder that affects millions of people around the world. Through years of study and research, it has concluded that the cause of the disease is the presence of 4 kDa amyloid protein (Maloney 2014). The A"β" protein serves as a trigger inducing hyper-phosphorylation of mictrotubule- associated protein t(MAPT) (Maloney 2014). However, the cause of the disease, resulting in damage to regions of the brain that deal with memory and cognition, is through the death of neurons and a “reduction in the levels of synaptic proteins in the regions in which the neurons terminate” (Bali 2010). The damage to these regions …show more content…
According to the hypothesis, there is an error in the processing of the amyloid precursor protein (APP), which leads to the production of beta-amyloid, a short fragment of the protein. The amyloid" β " - peptide accumulates in the brain triggering destruction of nerve cells resulting in the pathogenesis of Alzheimer’s Disease. Accumulation of beta amyloid leads to clumping in the tissue of the brain creating what is known as amyloid plaques (Kahn 1). The hypothesis indicates that beta amyloid is over produced in the brain, that there is fault in removing beta amyloid from the brain, or that both factors are at play, resulting in the accumulation of A"β" in the brain (Hardy …show more content…
Because A"β" is critical to the pathogenesis of Alzheimer’s disease, “it is imperative to understand the molecular and cellular basis of its production” (Bali 2010). The A"β" peptides themselves are formed from an Amyloid Precursor Protein, “ by the sequential action of of "β" - sycretase and "γ " secretase” and are released, forming plaques. The toxic properties of these plaques include the phosphorylation of tau, thus the creation of tangles in the brain, and neurodegeneration (Bali 2010). The Amyloid precursor protein is an “integral membrane protein with a large N-terminal extracellular domain and a short C-terminal cytoplasmic domain”, expressed ubiquitously, APP catabolically produces A"β" ( Bali 2010). The proteolytic processing of the precursor protein In order to combat Alzheimer’s Disease, researchers are looking to develop anti-Aβ strategies that would inhibit the production of A"β" . The development of a technique or drug that would curb A"β" , would decrease the clumping of peptides in the brain and therefore improve cognitive function in patients with the
The article “Cracking the Alzheimer’s code” by Linda Marsa discusses the history, discoveries and advancements for Alzheimer’s disease. The discovery of Alzheimer’s disease was revealed through a German physician named Alois Alzheimer. Alzheimer first discovered Alzheimer’s in the year 1901 while he was interviewing a mentally Ill patient named Auguste Dexter. The beginning of his discovery was due to the fact that Dexter was exhibiting uncontrollable behaviors that included jealously, screaming, confusion and paranoia. After Dexter had passed away, Alzheimer saw this as an opportunity to examine her brain under a microscope in thin pieces. To Alzheimer’s surprise, he discovered two abnormal substances on brain slices that were called amyloid
This approach can be very helpful for doctors and clinicians to find a cure for Alzheimer’s disease, but this disease varies a lot in each patient and they all might have a different cause of the disease (Begley et al., 2001). Many companies have started to offer stem cell treatment for this disease, however there is no evidence that it is an effective and safe treatment. A lot of scientists are considering the fact that one day stem cells will help cure and treat Alzheimer’s disease in another way, sooner than the advancement of potential stem cell transplant therapy. Using stem cells taken from Alzheimer’s patients, new treatments can be developed and it is a growing field of research.
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...
Lack of acetylcholine is the main cause for loss of memory. In most people throughout the aging process, acetylcholine degenerates over time at a normal rate. In people affected by Alzheimer’s, acetylcholine degenerates at more than double the rate of people unaffected with this disease. Acetylcholine is a major neurotransmitter in the brain that allows communication of information from one nerve cell to an...
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.
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 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)
...d up in lysosomes of the amyloid precursor protein (APP). Once broken, in an improper process, into toxic peptides which are associated with Alzheimer's Disease, researchers suggest they are perhaps a reason for the development of Alzheimer’s disease. Within weeks of using gene therapy to increase the activity of the NEU1 enzyme, it was found that plaque began to decline. The regions in which the researchers saw a decline in plaque was in the hippocampus.
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.
Thesis/Preview Statement – Alzheimer’s disease (AD) causes a decline in brain function, it destroys healthy nerve cells. Today, we have discussed Causes, Symptoms, and Diagnosis of AD.
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 ...
One of the most refutable arguments against the amyloid-beta theory is that a considerate amount of elders, particularly above 70 years of age, have amyloid plaques with no cognitive decline (Corrada et al., 2012). It is estimated that about 1/3 of old age persons without in vivo diagnosis of AD or any other dementia, have brain histopathological features
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.
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...