Buy research papers about als

Buy research papers about als

Buy A Research Paper Online,Essay about Als Outline

WebJun 24,  · ALS Research Paper Review. For Patients and Friends > ALS Research Paper Review. ALS Research Paper Review. The CReATe Consortium has partnered WebFeb 1,  · Mar. 29, — Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disorder that affects as many as 30, people in the United States, with 5, new WebOct 21,  · If someone is interested in learning more about ALS research and drug discovery, what kinds of research papers do you think they should be paying attention WebWith blogger.com you get research papers for sale quickly and hassle-free. Our research paper writing services will provide whichever type of academic assignment on WebIf you want to order a custom research paper writing service but don’t want to waste time doing it, you will be pleasantly surprised to learn that the order placement process on our Missing: als ... read more

Forgot password. Research Papers For Sale Order research papers are written by Experts. Place your order now. Proceed to Order. Order 1 page Order 1 page. Choose your writer PapersOwl expert writers are online and available for hire. Bard-Writers Team Completed orders: 4. Factors Affecting Economic Development in Third World Countries Paper Type: Essay Any Type Subject: Art Style: APA Sources: 0 Read sample. HIRE A WRITER. Completed orders: 4. Effects of Oil Spill Paper Type: Essay Any Type Subject: Environmental Issues Style: APA Sources: 1 Read sample. Doctor Brenda Completed orders: 4. Blockchain in logistics real-life use cases Paper Type: Essay Any Type Subject: Technology Style: APA Sources: 1 Read sample.

Dr Mary PhD Completed orders: 4. Sex Trafficking: A Multi-Billion Dollar Business Paper Type: Essay Any Type Subject: Criminology Style: APA Sources: 1 Read sample. Gama Completed orders: 4. Animal Testing Should Be Banned Paper Type: Essay Any Type Subject: Sociology Style: APA Sources: 1 Read sample. EssaysCaptain Completed orders: 4. About Cryptocurrency Paper Type: Essay Any Type Subject: Technology Style: APA Sources: 1 Read sample. Grace PhD Completed orders: 4. Paper Type: Essay Any Type Subject: Law Style: APA Sources: 1 Read sample. Dr Joe Phd Completed orders: 4. Cyber Security Threats in Healthcare Paper Type: Essay Any Type Subject: Technology Style: APA Sources: 1 Read sample. Prof Estella PhD Completed orders: 4. Childhood obesity parents are the blame Paper Type: Essay Any Type Subject: Medicine and Health Style: APA Sources: 1 Read sample.

Place Order. Research Paper Features. Styles Available. English MBA and Business Nursing History Psychology Management Sociology Biology Finance Chemistry Philosophy Engineering. Free for You. Order now. WHY CHOOSE US? Timely delivery. Professional writers. Privacy policy. Find out how much your paper will cost. Explore bids from our writers Explore bids from your phone. HOW TO PLACE AN ORDER FROM YOUR PHONE. PLACE AN ORDER. What citation style will you use to format my research paper? All of our personnel are familiar with the style guides used in American universities and colleges. The four most-common citation styles are APA, MLA, Harvard, and Chicago. We are also able to provide formatting in Oxford, CMS, AMA, ASA, IEEE, among others.

Let us know when you place your order what style your essay should adhere to. Are your writers experienced in my topic? The writers employed by our platform come from a variety of academic and professional backgrounds. June 24, PM CDT Dissecting ALS Research Articles: Dr. Franz Makes it Easier Speaker: Dr. Colin Franz, MD, PhD This educational webinar is hosted by the Les Turner Foundation and endorsed by ALS RPR. Click here to view webinar recording. Click here to view the roundtable recording Recommendation: Skip to 46ms. Phil was diagnosed with ALS in August of at the age of He is a graduate of the University of Washington where he was on the National Championship UW Football team.

He has spent the past 25 years building a career in developing technology solutions for brands such as Sony, Hewlett Packard, and Home Depot. A loving husband to his wife Jennifer, Phil is also a dedicated father to four children Arianne, Hunter, Parker, and Whitney After his diagnosis, he immediately dedicated himself to making a difference in the fight against this horrific disease. Phil is active in helping multiple ALS organizations with promoting ALS legislation and policy issues, increasing awareness and raising funds to find effective treatments and cures, and providing much-needed support services for ALS patients and families. Natalie has been active within the ALS community since , when her mother, Martha Olson-Fernandez, was diagnosed with bulbar onset ALS.

She is currently a board member of the Martha Olson-Fernandez Foundation MOFF , which is a c 3 foundation that Martha started in , shortly before she passed away. Today, MOFF funds ALS patient care on the Central Coast of CA and national ALS research projects. Natalie studied the economics of funding rare diseases while attending the MBA program at the Philadelphia College of Pharmacy. She is energized by the innovation that has emerged within the ALS scientific field over the last 8 years and is looking forward to witnessing more initiatives that close the gap between the content within scientific laboratories and viable treatment options for people living with ALS. Natalie currently works as the associate project manager of clinical development at Viracta Therapeutics in San Diego, CA.

Families of terminally ill patients suffer significant effects related to an illness, forcing some households to have large debts and making them unable to afford food and other necessaries. One specific terminal illness is called Amyotrophic Lateral Sclerosis ALS , also known as Lou Gehrig's disease. ALS is a disease affecting the human nervous system like the brain, muscles, and spinal cord. It is a deadly disease that cripples and kills its victims. ALS is a terminal illness that is characterized by specific symtoms and has treatments. The nerve cells in the brain and spinal cord that are responsible for sending and receiving motor signals progressively die off, causing the deterioration of simple motor skills in patients with ALS, such as walking, talking, and eventually speaking and breathing, however thinking is not affected by ALS.

Early symptoms cause the person to slowly lose mobility of limbs, but in a matter of a few years, the person loses the mobility of most of their body and will eventually lose the ability to eat and breath, which will ultimately cause death. ALS deteriorates the patient's body, however does not affect the patient's state of mind or sanity while the rest of the body shuts down. People usually get ALS between the ages of 40 and However, there is a growing trend where athletes are getting ALS in their thirties. In recent studies, however, it was observed that individuals who have had suffered multiple concussions or any other head trauma are.

Each year approximately 5, people are diagnosed with ALS, and statistics show that there are nearly 20, Americans who have it at any given time. French neurologist Jean-Martin Charcot is believed to be the scientist who discovered the disease in With someone who has ALS, their muscles are receiving no nourishment, therefore it withers away. To explain the loss of There are motor neurons that reach from the brain to the spinal cord and from the spinal. This disease is a progressive neurodegenerative disease that causes muscle weakness, paralysis, and ultimately, respiratory failure. This disease has a lot of awareness from the world. Lots of people donate money , and have also done the ALS ice water bucket challenge.

Imagine you are a year-old man, a beloved professor from Brandeis University. Every day you take notice of the increased difficulty of breathing, more so than the usual, or the out-of-breath feeling from climbing a flight of stairs. After multiple testing, your results come back and you have ALS, also known as Amyotrophic lateral sclerosis. The National Institute of Neurological Disorders and Stroke have identified over 12 genetic mutations as the cause in some familial cases of ALS. htm Personally speaking, when I told my mom about the ALS Ice Bucket Challenge, she told me that ALS was what my great grandma had died from.

Unfortunately for my great grandma and the others suffering from ALS, there has not been a cure found yet for ALS. There is one FDA approved drug for ALS called riluzole Rilutek. Riluzole helps to reduce the damage to the nerves that are being attacked by the disease. Amyotrophic Lateral Sclerosis ALS is a terminal disease, also known as Motor Neurons Disease, Charchot Disease and Lou Gehrig disease. ALS destroys the Central Nervous System CNS and causes damage to the upper and lower motor neurons in the brain. Signs and symptoms are characterized as: muscles weakness, muscle atrophy, twitching and reduced muscle reflexes.

Eventually the patient will become paralyzed and rely on a tracheostomy and ventilator for breathing ALS Association [ALSA], Overtime, the symptoms will. Musculr Dystrophy Assocation. There is no clear-cut time frame for how long somebody has after they get diagnosed with this disease. Some peoples symptoms gradually grow over time, others occur rapidly, and then plateau.

Intense research is being conducted in many areas related to ALS, from basic science seeking the roots of the disease to therapy development to find effective treatments. Research into familial running in families forms of the disease also may have relevance for sporadic nonfamilial forms, as all ALS cases,regardless of the form, may present and develop along similar lines. This section offers an overview and links to more information about ALS research targets and strategies, and research administration in ALS. Additionally, there are many strategies currently in the pipeline for ALS drug development.

Read about the ALS research MDA has recently funded and also check out recent news about research. Many genes, when mutated, can cause familial ALS. Among them are the SOD1 gene, the TDP43 gene and the FUS gene. Defects in the C9ORF72 gene were also shown to cause another disease called frontotemporal dementia FTD. Some patients with the gene defect develop ALS, some develop FTD, and some patients develop symptoms of both diseases. Other genes shown to contribute to rare forms of ALS include ubiquilin 2, profilin 1, valosin-containing protein, alsin, senataxin, angiogenin, and optineurin. If someone with an ALS-causing gene mutation is the first in the family to show the disease, the disorder is classified as sporadic because there is no family history.

This can happen when, for example, a parent carrying the ALS-causing mutation passes away of other causes before ALS develops but not before passing the mutation along to his or her children. However, research on the genetic factors that contribute to ALS, without necessarily causing it directly, is of great interest. Scientists suspect that a number of gene variants, in combination with other unknown factors, may increase susceptibility to sporadic ALS. Several large gene association studies have been done comparing the DNA of people with and without ALS in hopes of uncovering genetic differences. These studies have pointed toward potential genetic targets for ALS research.

When scientists studied DNA from people with ALS and without the disease, they found expanded ataxin 2 genes in 43 4. They concluded that ataxin 2 expansions are significantly correlated with increased risk for developing ALS. Expanded ataxin 2 protein molecules appear to have toxic interactions with TDP, another protein implicated in ALS, and blocking ataxin 2 interactions with TDP could become a new therapeutic avenue. There are several approaches in development to treat genetic versions of ALS including familial ALS caused by SOD1 mutations and C9ORF72 expansions. One strategy involves development of a drug called an antisense oligonucleotide ASO , which is able to block defective SOD1.

While the first-generation ASO was determined to need adjustments to improve its potency, these early studies were landmark since this was the first trial testing an ASO in neuromuscular disease through intrathecal injection into the spinal canal delivery and paved the way for the trials currently in progress. Biogen has licensed the SOD1 ASO from Ionis Pharmaceuticals and is continuing clinical testing of this therapy. In ALS, there is some evidence that excess amounts of the neurotransmitter glutamate accumulate in the spaces around a nerve cell after it has completed its signaling function, causing problems for nerve cells in the vicinity. Normally, glutamate, a chemical transmitter of signals between nerve cells, is released by a sending neuron and docks on a receiving neuron.

Once docked, it is quickly cleared away by glutamate transporter proteins, which are produced by neighboring cells in the nervous system called astrocytes. In ALS, something may go wrong with this glutamate clearance system. Some studies have suggested that, in ALS, a protein called EAAT2 a glutamate transporter may not be as efficient at clearing glutamate away from nerve cells as it should be. Other studies have suggested that a glutamate receptor, a docking site on the surface of motor neurons that receives glutamate, may be excessively permeable in this disease. A drug specifically approved for the treatment of ALS by the U. Food and Drug Administration FDA is riluzole Rilutek , which is believed to interfere with the action of glutamate.

However, other drugs affecting glutamate neurotransmission have not been successful in clinical trials. There is a growing body of evidence that malfunction of the immune system is at least part of the ALS disease process. Research has identified abnormal immune system overactivity in animal models of the disease, and investigators have observed it in blood samples from people with ALS. It had been thought that motor neurons died on their own in ALS. But, today, there is evidence that immune system cells in the nervous system called microglia are involved in their demise. Blocking or modifying parts of the immune system is a strategy being pursued in several clinical trials for ALS.

While some research teams have focused their attention on microglia, the nervous system's immune cells, others have focused more on astrocytes , a type of non-nerve glial cell that normally provides support to motor neurons and other cells in the nervous system. Among their roles is clearing away a potentially toxic compound called glutamate from the area around and between nerve cells. These cells acquire pathologic activity, and in experimental models, astrocytes proved to be responsible for motor neuron death. Investigators have shown that treating astrocytes alone can delay disease onset and extend survival in mice with a disease resembling ALS caused by mutations in the SOD1 gene.

Currently, there are several laboratories working to understand how astrocytes become dysfunctional in ALS and develop therapies targeting astrocytes in ALS patients. Cellular proteins normally fold only in certain ways shortly after they're produced. When folding goes wrong, the result may be a highly toxic protein. In , researchers found that misfolded SOD1 protein, unaccompanied by an SOD1 gene mutation, could be found in at least some cases of sporadic ALS. Other proteins besides SOD1 may misfold and contribute to the disease as well.

For example, the TDP proteins appear to misfold and form clumps aggregate in ALS-affected motor neurons even when the genes for these proteins are normal. TDP aggregates have been found in the nervous system tissue for the majority of types of ALS. TDP regulates the expression levels of hundreds of RNAs, many of which play important roles in neuronal function. One of these, stathmin-2, appears to be critical for axon regeneration, and altering TDP function prevents stathmin-2 from repairing damaged axons. Because axonal degeneration of motor neurons is a key feature of ALS pathogenesis, rescuing stathmin-2 levels has emerged as a very promising therapeutic target.

Normally, proteins called chaperones help coax other proteins to fold into the correct shape. Therefore, some scientists are working on increasing levels of these chaperone proteins. In ALS, the cellular "energy factories" called mitochondria malfunction, although it isn't clear exactly where in the chain of events of the ALS disease process this malfunction occurs. When mitochondria malfunction, they may fail to produce the needed energy for cells, and they may leak toxic substances called reactive oxygen species , subjecting cells to a kind of poisoning known as oxidative stress. The U. Food and Drug Administration on May 5, , approved Edaravone brand name Radicava for the treatment of ALS.

Radicava is thought to work by relieving the effects of oxidative stress. Targeting this pathway could potentially preserve motor neuron health, which could, in turn, keep muscles functional for a longer period of time. For more, see FDA Approves Radicava to Treat ALS and Questions and Answers About Newly FDA-Approved Radicava to Treat ALS. Unfortunately, coenzyme Q10, which combats oxidative stress, was not found to be helpful in people with ALS, even at high doses. Coenzyme Q10 is an antioxidant , which is a substance that helps clean up free radicals.

MDA-supported researchers continue to study mitochondrial dysfunction in ALS, with an eye to determining whether it is a cause or a consequence of motor neuron loss and whether restoring mitochondrial function can alter the ALS disease course. Stem cells can be thought of as cells that are in the very early stages of development, before they become specialized differentiated to perform specific roles in tissues. They may be precursors to a specific cell types such as muscle or nerve cells , or they may still retain pluripotency the ability to develop into any cell types. Stem cell research is an evolving field that may potentially benefit people affected by neuromuscular disease. There are many different types of stem cells used in biological research.

One new type of stem cell is called the induced pluripotent stem cell iPSC. These stem cells are unique in that they have the regenerative capabilities of embryonic stem cells they are not created by destroying human embryos. Rather, scientists have discovered methods to create iPSCs in the lab using human skin or blood as a starting source. Induced pluripotent stem cells iPSCs have the potential to make most, if not all, tissue types of the body similar to an embryonic stem cell. Therefore, they are being widely used by scientists to model disease in a dish and are particularly helpful for diseases affecting tissues like the brain and spinal cord e.

ALS mainly since it is difficult to take biopsies of the affected tissues. Adult stem cells are a type of stem cell found in all living humans which help to regenerate or repair the body throughout life. Adult stem cells have been found in many tissues including muscle, brain, and bone. These types of stem cells are currently under investigation for their potential to repair, regenerate, and nourish the muscles and nerves damaged in neuromuscular disease. Stem cells also are in development as cell-transplantation therapies. In ALS, stem cells are being tested in multiple clinical trials for their nourishing abilities to help ailing nerve cells.

Many companies and institutions outside the United States and a few inside falsely advertise that they can cure ALS with stem cells. So far, there are no FDA-approved stem-cell-based treatments for ALS, and therefore stem cell therapies should be approached with great caution. Vascular endothelial growth factor VEGF is a signaling protein that stimulates growth of new blood vessels. It has been shown that that patients who have genetic variants in the VEGF gene may be more susceptible to ALS has increased enthusiasm for the possible role of growth factors in this disease. Furthermore, studies in a mouse model that does not produce VEFG show that treatment of this animal with VEGF has resulted in significant improvement.

Apoptosis, also known as programmed cell death pathway, is an orderly and necessary way of clearing old cells and maintaining balance in the body. In some cases, apoptosis can become dysregulated, and that can lead to disease. Some evidence suggests that apoptosis may be a late pathway for motor neuron degeneration in ALS. There is evidence that inhibition of this programmed cell death pathway in a mouse model of ALS halted neuronal loss and prevented axonal degeneration, symptom onset, and paralysis. Survival was extended in this animal model. These findings suggest that inhibition of apoptosis is a possible therapeutic strategy for ALS. A wide range of agents targeting different aspects of the pathophysiology of ALS are being explored in both sporadic and familial ALS. This clinical data will be married with genetic and patient-reported information to generate a hub of valuable real-world information.

Through MOVR neuroMuscular ObserVational Research , MDA will accelerate the development of new treatments and improve the health outcomes for patients with neuromuscular disease. MOVR Data Hub ties its origins to the original MDA registry launched in , and has collected clinical data from more than 3, patients with ALS, BMD, DMD, and SMA. The pilot phase allowed MDA to gain insights and learn best practices for a multi-disease national neuromuscular disease registry. Systematic collection and rigorous management of clinical, genetic, and patient-reported data in combination with preparing the community for more clinical trials will power continued research, clinical development, and treatment advancement.

To learn more, click here. In , the U. Centers for Disease Control and Prevention opened the National ALS Registry to compile a large database of information about the incidence and prevalence of ALS, how the disease develops, and what types of treatments and interventions are beneficial. Participation in the registry will help researchers understand whether some types of ALS are caused by environmental hazards, geographic exposures, or occupational risks.

ALS Research Papers,WHY CHOOSE US?

WebAmyotrophic Lateral Sclerosis (ALS) is a motor neuron disease that has been known to physicians since the late ’s. ALS was first discovered in by French neurologist WebJun 24,  · ALS Research Paper Review. For Patients and Friends > ALS Research Paper Review. ALS Research Paper Review. The CReATe Consortium has partnered WebALS Research Papers Lateral Sclerosis (ALS) is a motor neuron disease that has been known to physicians since the late ’s. ALS was first discovered in by French WebOct 21,  · If someone is interested in learning more about ALS research and drug discovery, what kinds of research papers do you think they should be paying attention WebJun 15,  · Disease Research Paper: Lou Gehrig’s Disease / ALS (Amyotrophic Lateral Sclerosis) ALS (Amyotrophic Lateral Sclerosis) or Lou Gehrig’s Disease is WebWith blogger.com you get research papers for sale quickly and hassle-free. Our research paper writing services will provide whichever type of academic assignment on ... read more

This flips a long-standing belief the disease starts in the spinal motor neurons and any Place Order. Campaign Cookies Checkbox Campaign Cookies. Patients with Amyotrophic Lateral Sclerosis Have High Interest in and Limited Access to Genetic Testing external icon. Bard-Writers Team Completed orders: 4. English MBA and Business Nursing History Psychology Management Sociology Biology Finance Chemistry Philosophy Engineering.

Right to Die Ethical Case Analysis. June 30, — Amyotrophic lateral sclerosis, or ALS, attacks nerve cells known as motor neurons in the brain and spinal cord, gradually leading to paralysis. Fernando Vieira, buy research papers about als. Prevalence of Amyotrophic Lateral Sclerosis — United States, And getting any service that makes your life simpler and tasks done correctly is typical. Fill out an order form and include as much detail as possible. ALS Research Paper Review.