...The Study Of Alzheimer’s What exactly is Alzheimer’s disease? Alzheimer’s disease is a disorder that occurs in the brain in which specific brain cells degenerate, causing memory loss, and impairs thinking and behavior. It usually develops in people in their 60’s or early 70”s, and approximately 4 million Americans suffer from this disease and 100 million die each year. The risk factors for developing Alzheimer’s disease: There are 3 genes when mutated that cause Alzheimer’s disease. * APP gene (amyloid precursor protein) (chromosome 21) is expressed in the synapse and is thought to be responsible for forming and repairing synapses. Mutations of the APP gene have been associated with Alzheimer ’s disease and with early onset in particular. A primary cause of Alzheimer’s disease is deposits of a protein called amyloid-beta as plaques in the brain. Beta amyloid is released following cleavage of APP at a number of points, and mutations can lead to an increase in production of protein. More than 20 mutations of the APP gene haven been and cause early onset of Alzheimer’s disease. * Presenilin 1 gene (chromosome 14) and Presenilin 2 gene ( chromosome 19) are proteins that span the cell membrane and are primarily expressed in neurons. They also determine secretase activity, which is responsible for cleaving the amyloid precursor protein (APP). In sum APP cleavage can produce amyloid-beta, which is the primary component of plaques in the brains of Alzheimer patients...
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...Alzheimer’s disease is characterized as a type of irreversible dementia that causes problems with memory, thinking, and behavior which can affect the ability to perform simple tasks. (Alzheimer’s Association). Unfortunately, Alzheimer's is the sixth leading cause of death in the United States and over five million Americans are currently living with Alzheimer’s (National Institute of Aging). Each of the three categories of Alzheimer’s has unique symptoms. In mild Alzheimer’s disease, where Alzheimer’s is usually diagnosed, the person presents with memory loss and other problems such as behavior changes and taking longer to complete activities of daily living. In moderate Alzheimer’s, the person begins to have damage to parts of the brain that...
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...Neurodegenerative Disorders: Alzheimer’s Disease 1. Amyloid Precursor Protein (APP) Alzheimer’s disease (AD) remains a major cause of senile dementia, which is characterised by an impairment of neuronal and synaptic function in addition to the accumulation of β-amyloid plaque and formation of neurofibrillary tangles within distinct portions of the brain (De Strooper and Annaert, 2000). Progression of this distinct pathology of neurodegeneration does not typically vary from patient to patient, beginning in cerebral cortex before targeting the hippocampus, neocortex as well as the sub-cortical nuclei (Braak and Braak, 1995). The role of amyloid precursor protein (APP) in the pathogenesis of Alzheimer’s disease is pivotal. The cleavage of APP by the proteases β and γ- secretase releases β-amyloid (Aβ) peptides which results in aggregation of the peptides due to misfolding to form fibrils of Aβ which comprise the key components of amyloid plaque deposits in the brains of AD patients (Glenner and Wong, 1984). Amyloid precursor protein (APP) is a trans-membrane glycoprotein which normally functions in synapse formation as well as axonal elongation. The protein possesses a small cytoplasmic domain but is composed primarily of a large extracellular domain. Processing of APP in the extracellular domain by α or β- secretase results in the complete removal of the protein’s ectodomain which gives rise to an accumulation of sizeable and soluble derivatives of APP referred to as...
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...brain is made up neurons that are interconnected to form a vase network. These connections known as synapses enable the transmission of information from one neuron to another. In Alzheimer’s disease, ten to fifteen years before the appearance of the symptoms, two main lesions form in the brain, which are senile plaque’s that are composed of Beta-Amyloid protein, and neurofibrillary tangle’s that are composed of Tau protein. On the surface of a neuron is a large protein called APP. Normally, APP is sectioned by enzymes on the surface of the neuron and it frees a protein called Amyloid-Beta. The amyloid-beta protein is then cleared in the body. In the case of Alzheimer’s disease there is an imbalance as the amyloid-beta protein is no longer regulated and is found in two greater quantities. The protein is assembled to form insoluble fibrils and create Senile Plaques. When a neuron communicates with another a signal goes from the body known as soma to the synapse to transfer the information. The signal passes through the skeleton of the neuron composed of microtubules. These microtubules are stabilized by normal towel protein. In Alzheimer’s disease, Tau protein becomes defective and detaches from the microtubules. Thus, the skeleton of the neuron dissociates, as it is no longer maintained. Defective tau protein is then assembled to form filaments in the neuron. Without the skeleton the neurons degenerate and connections between the neurons are lost. The abnormal accumulation of Tau filaments...
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...Alzheimer's disease is the most common cause of dementia. The word dementia describes a set of symptoms that can include memory loss and difficulties with thinking, problem-solving or language. These symptoms occur when the brain is damaged by certain diseases, including Alzheimer's disease. This factsheet describes the symptoms of Alzheimer's disease, how it is diagnosed, and the factors that can put someone at risk of developing it. It also describes the treatments and support that are currently available. Alzheimer's disease, named after the doctor who first described it (Alois Alzheimer), is a physical disease that affects the brain. There are more than 520,000 people in the UK with Alzheimer's disease. During the course of the disease,...
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...Alzheimer's Disease and its Link to the Normal Human Developmental Process of Aging Angel M. Perez Liberty University Abstract The cause of Alzheimer’s disease (AD) is currently unknown. However, extensive studies using new technology has led to new ways of accurately identifying AD, an understanding of the mechanisms involved regarding the development of AD, and the damage it causes in the human brain. The general population is under the impression that AD is a result of the normal human developmental process of aging. The focus of this research is to dismiss this misconception by providing indisputable empirical evidence to the contrary. This paper looks at the various studies explored by researchers in an attempt to show the factors attributed to AD, a population over the age of 65 that do not suffer from AD, and a population of as young as 18 clinically diagnosed with Alzheimer's disease. The author also addresses life style, environmental, and genetic risk factors attributed to the development of AD. Alzheimer's Disease and its Link to the Normal Human Developmental Process of Aging Contrary to popular belief, studies show that Alzheimer’s disease is not part of the normal human developmental process of aging. It is imperative that researchers acknowledge that AD is not part of the normal aging process. Researchers must keep an open mind during the research and experimental process, exploring all plausible arguments, in order to discover the cause(s) and/or...
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...Final Research Paper Ryan Hermes Health 106 SP 13 “Alzheimer’s Disease; A Disease Without A Cure” Alzheimer’s disease, otherwise known as dementia, is a genetic disease that causes the brain to deteriorate until death. Currently, there is no cure for Alzheimer’s disease, and once the diagnosis is given the disease only gets worse. The disease isn’t very well understood, however researchers are working to help treat the symptoms of the disease. With all of the advancements in medicine there are no treatments available to stop or reverse the progression of Alzheimer’s disease. In 1901 a German psychiatrist named Alois Alzheimer’s documented the first recorded case of Alzheimer’s disease. He studied a woman named Auguste Deter, she was a woman in her fifties who had severe early onset Alzheimer’s disease, and she died in 1906. After her death, Alzheimer’s worked with two Italian physicians on staining techniques to study Auguste’s brain. He noted certain plaques that infiltrated her brain, however technology could only go so far at the time so the results of the brain examination were speculative. Alzheimer’s disease affects the brain in a way that causes its victims to lose some or most of their memory. This causes the patient to forget things such as who they are, who their relatives are, where they are, how to get home, or even when or how to eat. These problems make caring for the patient difficult because the care person has to do almost everything...
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...neurodegenerative diseases is the progressive accumulation of nuclear inclusions comprising of irregularly folded protein aggregates. Previously it was thought that protein aggregation is the cause of neurodegeneration as it had been established that neurodegenerative diseases such Huntington’s disease (HD), Parkinson’s disease (PD), Alzheimer’s disease (AD), prion disease, and amyotrophic lateral sclerosis (ALS) all shared a common feature which was these aggregated proteins and the formation of inclusion bodies (Ross and Poirier, 2004). However, recent studies have suggested that protein aggregation may not be the cause of toxicity to cells but that it may in fact be a protective mechanism. The aggregates formed in the above-mentioned diseases can be a consequence of mutations in the sequence of the protein that is related to the disease, increased amounts of a normal protein due to a genetic variation, or even the absence of genetic variations. These may be initiated by environmental stress or aging (Ross and Margolis, 2005). The aggregated proteins can build up and form inclusion bodies, which can be either intracellular or extracellular. There is an ongoing debate about the role of aggregation in the disease process even though one of the most common pathological features of neurodegenerative disorders is inclusion bodies. There is much evidence indicating that aggregation is associated with toxicity in these diseases. On the other hand, there are those studies that have suggested...
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...individuals in the US, Alzheimer’s affects 5.3 million Americans, like president Ronald Regan . Alzheimer’s disease (AD) is the most common of dementia and rises steeply with age . AD is a progressive mental deterioration of the brain where the disease attacks the brain’s nerve cells, which results in progressive thinking, judgment, and memory loss . These symptoms last for decades. Eventually, individuals with this disease will be unable to remember facts, family members or events . Unfortunately, Alzheimer’s will kill the diseased person. Changes in the brain, which are caused by Alzheimer’s, contribute to the death of the individual, but the...
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...mellitus is a syndrome with disordered metabolism and inappropriate hyperglycemia due to either a deficiency of insulin secretion or to a combination of insulin resistance and inadequate insulin secretion to compensate. Diabetes mellitus occurs in two primary forms: type 1, characterized by absolute insufficiency, and the more prevalent type 2, characterized by insulin resistance with varying degrees of insulin secretory defects. Diabetes mellitus is a group of metabolic diseases characterized by elevated levels of glucose in the blood (hyperglycemia) resulting from defects in insulin secretion, insulin action, or both (ADA], Expert Committee on the Diagnosis and Classification of Diabetes Mellitus, 2003. Causes for Diabetes Mellitus The cause of both type 1 and type 2 diabetes remains unknown, although genetic factors may play a role. Diabetes mellitus results from insulin deficiency or resistance. Insulin transports glucose into the cell for use as energy and storage as glycogen. It also stimulates protein synthesis and free fatty acid storage. Insulin deficiency or resistance compromises the body tissues’ access to essential nutrients for fuel and storage. The resulting hyperglycemia can damage many of the body’s organs and tissues. Type 1 diabetes is due to pancreatic islet B cell destruction predominantly by an autoimmune process, and these patients are prone to ketoacidosis. Type 2 diabetes is the more prevalent form and results from insulin resistance with a defect...
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...Esperanza Morato1, Alberto Rábano2, Izaskun Rodal2, Luis Carrasco1 Corresponding address 1. Centro de Biología Molecular “Severo Ochoa”. c/Nicolás Cabrera, 1. Universidad Autónoma de Madrid. Cantoblanco. 28049 Madrid. Spain. 2. Department of Neuropathology and Tissue Bank, Unidad de Investigación Proyecto Alzheimer, Fundación CIEN, Instituto de Salud Carlos III, Madrid. Spain. How to cite this article: Alonso R, Pisa D, Marina AI, Morato E, Rábano A, Rodal I, Carrasco L. Evidence for Fungal Infection in Cerebrospinal Fluid and Brain Tissue from Patients with Amyotrophic Lateral Sclerosis. Int J Biol Sci 2015; 11(5):546-558. doi:10.7150/ijbs.11084. Available from http://www.ijbs.com/v11p0546.htm Abstract Among neurogenerative diseases, amyotrophic lateral sclerosis (ALS) is a fatal illness characterized by a progressive motor neuron dysfunction in the motor cortex, brainstem and spinal cord. ALS is the most...
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...PCB 3702 Chapter 8 The Central Nervous System Learning Objectives 1. Describe the embryonic origin of the CNS 2. Identify the 5 brain regions & the major structures they contain, including the ventricles 3. Describe the organization of the sensory & motor areas of the cerebral cortex, & the nature of the basal ganglia 4. Distinguish between the functions of the right & left cerebral hemispheres, and describe the significance of the limbic system 5. Identify the areas of cerebral cortex involved in speech & language 6. Describe the brain regions involved in memory and events associated with learning & language Learning Objectives 7. Describe the locations & functions of the thalamus & hypothalamus 8. Identify the structures & functions of the midbrain & hindbrain 9. Describe the structure & function of the RAS 10. Describe the sensory & motor pathways 11. Describe the structure & function of the pyramidal & extrapyramidal motor tracts 12. Identify the structures of a spinal nerve and describe the neural pathways of a reflex arc. I. Structural Organization of the Brain A. Central Nervous System 1. Composed of the brain and spinal cord a. Receives input from sensory neurons and directs activity of motor neurons that innervate muscles and glands b. Association neurons integrate sensory information and help direct the appropriate response to maintain homeostasis and respond to the environment. Central Nervous System Gyrus ...
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...M.N.V. Ravi Kumar ⁎ Department of Pharmaceutics, National Institute of Pharmaceutical Education and Research (NIPER), Phase-X, S.A.S. Nagar, Mohali, Punjab, India - 160062 Received 31 January 2006; accepted 26 April 2006 Available online 13 May 2006 Abstract Antioxidants are emerging as prophylactic and therapeutic agents. These are the agents, which scavenge free radicals otherwise reactive oxygen species and prevent the damage caused by them. Free radicals have been associated with pathogenesis of various disorders like cancer, diabetes, cardiovascular diseases, autoimmune diseases, neurodegenerative disorders and are implicated in aging. Several antioxidants like SOD, CAT, epigallocatechin-3-O-gallate, lycopene, ellagic acid, coenzyme Q10, indole-3-carbinol, genistein, quercetin, vitamin C and vitamin E have been found to be pharmacologically active as prophylactic and therapeutic agents for above mentioned diseases. Antioxidants are part of diet but their bioavailability through dietary supplementation depends on several factors. This major drawback of dietary agents may be due to one or many of the several factors like poor solubility, inefficient permeability, instability due to storage of food, first pass effect and GI degradation. Conventional dosage forms may not result in efficient formulation owing to their poor biopharmaceutical properties. Principles of novel drug delivery systems need to be applied to significantly improve the performance of antioxidants. Novel...
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...NOTE: This PDF document has a handy set of “bookmarks” for it, which are accessible by pressing the Bookmarks tab on the left side of this window. ***************************************************** We are the last. The last generation to be unaugmented. The last generation to be intellectually alone. The last generation to be limited by our bodies. We are the first. The first generation to be augmented. The first generation to be intellectually together. The first generation to be limited only by our imaginations. We stand both before and after, balancing on the razor edge of the Event Horizon of the Singularity. That this sublime juxtapositional tautology has gone unnoticed until now is itself remarkable. We're so exquisitely privileged to be living in this time, to be born right on the precipice of the greatest paradigm shift in human history, the only thing that approaches the importance of that reality is finding like minds that realize the same, and being able to make some connection with them. If these books have influenced you the same way that they have us, we invite your contact at the email addresses listed below. Enjoy, Michael Beight, piman_314@yahoo.com Steven Reddell, cronyx@gmail.com Here are some new links that we’ve found interesting: KurzweilAI.net News articles, essays, and discussion on the latest topics in technology and accelerating intelligence. SingInst.org The Singularity Institute for Artificial Intelligence: think tank devoted to increasing...
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