Health Essays Alzheimer Dementia Disease Essay

Health Essays Alzheimer Dementia Disease EssayAlzheimer Dementia ratiocination in on AlzheimersSoon, Alzheimers complaint go out touch everyone in this country in some form or a nonher, so the need to redouble our look for efforts greater than ever before. We moldiness mother better discussions, earlier detection, and effective strategies to continue Alzheimers. Scientists have made tremendous strides in the eventually two decades, but the clock is ticking. -Samuel Gandy, MD, PhD, chair of the Alzheimers Associations Medical and Scientific informative Council.There is no cure, but there is hope, for the worlds most leading arrest of dementiaALZHEIMERS.AD is a neuro chronic disorder, the underlying cause still being unknown. The clinical features or the underlying pathology can however be discovered on autopsy and thus the signs and indications of AD are instigated only after long time of accretion of the credible causes. Some of the signs take on-Cognitive deterioration. Visual spatial confusion.Loss of recognition of someones and objects. decrease mobility.Deterioration of muscles.Inability to feed oneself.Language disorientation.The onus of the illness lies in the deposition of fibrillized plaques containing granulose beta(AB).The AB proposition shows voltage for the reason that, as seen in patients with trisomy 21(downs syndrome), who have an additional copy of the gene for AB predecessor, almost universally exhibit AD like indications prior to age 40.These signs of AD can be accredited to the cyto harmful potential of the mature aggregated amyloid fibrils. Consequently, a great measure of the research work on lead breakthrough is focused on-Inhibition of fibrillization.Inhibition of AB precursor to AB.A different supposition understood to elicit the disease cascade, is centered on the personal effects of aggregated tau proteins. This speculation is sustained by the long standing observation that aggregation of AB plaques does not correlate d with neuron neediness.Although a great deal is known a propos the disease prognosis, causative or run a riskiness factors, the acquaintance we encompass of, in the present day, concerning the fundamental pathological origin or the core cause of the disease is zilch. Nevertheless, ApoE4, the foremost genetic risk factor for AD has been allied with surplus of AB build-up.The risk factors for AD are-Advancing age.Head injury.Aluminum intake.ApoE4.Poor CVS health.Smoking.AD is most often accomplished based on clinical signs and symptoms, and the history of patients infirmity, as a definitive diagnosis is only achievable by performing an autopsy. Common diagnostic tests include-Memory testing.Intellectual functioning.neuropsychological screening tests.Blood tests to rule out presence of other diseases.Functional neuro-imaging techniques like SPECT ad PET. one time diagnosed, on an average, survival is 7 10 years, the extremes being 4 years to 21 years.Essentials, statistics and incidence of Alzheimers-24 million pack affected with AD worldwide.Slated to become 81 million by 2040.1 out of 8 people above the age of 65 have AD.Only 19% with AD have the diagnosis recorded in their medical records.7th leading cause of death in the United States.From 2000-2004, death rate due to AD has increased by 32.8%, while that of breast cancer, prostate gland cancer, stroke and heart disease has decreased by 2.6, 6.3, 10.4, 8% respectively.Costs of AD and other dementias add to $148 billion annually.Current drugs in the global market for finenessment of Alzheimers-1ARICEPTKey essentials about ariceptWas permitted for the hold dearment of mild to moderate Alzheimers by the FDA in 1996, and for the treatment of severe Alzheimers in 2006 Is the 1 prescribed Alzheimers drugworldwide, more than 3.8 million people have been treated with Aricept. Aricept is a drug branded as a cholinesterase moderateor. It is one of a group of prescriptions that appear to improve the cogniti ve ability (thinking, perception, judgment and recognition) in people with Alzheimers disease. Aricept can reduce behavioral troubles that whitethorn be exhibited by people with this quality of dementia. Known as a cholinesterase inhibitor, Aricept delays the breakdown of the neurotransmitter acetylcholine in the brain. Acetylcholine helps communication between the human face cells and is vital for memory. grimace effects are typically mild and tend to disappear as treatment progresses. Common human face effects are nausea, vomiting, diarrhea, fatigue, insomnia, muscle cramps. Less common effects are headaches and dizziness. Rare side effects are anorexia, gastric or duodenal ulcers, gastro-intestinal hemorrhage, bladder overflow obstruction, liver damage, convulsions, heart problems and psychiatric disturbances. 2EBIXAEbixa exquisitely pointsEbixa is one of a group of drugs called NMDA (n-methyl-D-aspartate) receptor antagonists. These receptors, along with the neurotransmitte r glutamate, are implicated in transmitting case signals in the brain that may be imperative for teaching and memory. Ebixa, which acts on NMDA receptors, facilitates to normalize transmission of nerve signals, and perhaps slow the decline of some indications of Alzheimers disease. Ebixa is not a cure for Alzheimers disease as it does not affect the fundamental degenerative progression of the disease. Ebixa may cause some unwelcome re natural processs. These may include fatigue, dizziness, sleepiness, headache, hypertension (high blood pressure), constipation, vomiting, anxiety, confusion, hallucinations and sleep disturbance.3EXELONExelon particularsExelon is one of a group of drugs known as cholinesterase inhibitors which is intended to treat symptoms in people with mild to moderate Alzheimers disease. Exelon works by reducing the breakdown of acetylcholine and thus escalating the amount of the chemical in the brain, a chemical thought to be vital for learning and memory. The pr escription augments the action of acetylcholine by making the receptors it interacts with in the brain more responsive. Exelon is not a cure for Alzheimers disease as it does not affect the fundamental degenerative progression of the disease. Familiar side effects, in addition to nausea, vomiting, loss of appetite and weight loss, comprise of diarrhea, heartburn, stomach pains, dizziness, headache, weakness, fatigue and difficulty sleeping. A small number of people also experienced fainting.3REMINYLKey specifics on reminylReminyl ER is one of a group of drugs called cholinesterase inhibitors which is used to treat symptoms in people with mild to moderate Alzheimers disease. As of June, 2006, Reminyl became on tap(predicate) only in the extended put down (ER) format. It means that if you were taking Reminyl tablets twice a day prior to June 2006, you would now take a Reminyl ER capsule once a day. It augments the action of acetylcholine by making the receptors it interacts with in the brain more responsive. In the area of the brain first affected by Alzheimers disease, that dealing with cognition and memory, too little acetylcholine is available at the junctions between nerve cells to get messages across to the next nerve cell, The condition is helped, consequently, not only by preserving the acetylcholine from being destroyed by cholinesterase, but by making the receptors more responsive to the middle-level amounts of acetylcholine. Reminyl ER is not a cure for Alzheimers disease as it does not affect the fundamental degenerative progression of the disease. probable side effects include abdominal pain, diarrhea, indigestion, decreased appetite, difficulty swallowing, bleeding in the digestive system, weight loss, low blood potassium, low blood pressure, dehydration, seizures, agitation, aggression, hallucinations, weakness, fever, malaise, leg cramps, tingling in the pass on or feet, ringing in the ears, headache, dizziness, tiredness, sleeplessness, runny nose, urinary tract infection, fainting or fluttering of the heart.INTERNATIONAL food market STATISTICS FOR DRUGS USED IN THE TREATMENT OF ALZHEIMERSBRANDGENERICCLASSSPONSORSALES in (million $)2004 marketplace SHARE(approx)20042005AriceptdonepezilCIPfizer1,2661,58058.10%ReminylgalantamineCIJJ25634312.60%ExelonrivastigimineCINovartis32034012.50%NamendamemantineNMDAAForest52479.10%EbixamemantineNMDAALundbeck28863.20%AxuramemantineNMDAAMerz6150.60%CognextacrineCIFirstHorizon110.00%Others871073.90%TOTAL1,9692,719100.00%Total Sales Figures = $2.7B (2005) with Aricepthaving 58% market share.DRUGS IN stemma-Name of the drugsponsorphaseAbout the drugData from previous phases.FLURIZANMyriad3It is a selective amyloid lowering agent (SALA) that reduces levels of the toxic peptide amyloid beta 42 (A42).Reduces the levels of the toxic amyloid beta 42 peptide through the allosteric modulation of gamma-secretase.FLURIZAN has completed Phase2 human clinical trial in 207 patients with Alzheimers disease.Phase 1 safety trial of FLURIZAN in healthy older volunteers identified no proficient drug-related side effects.In nonclinical studies, FLURIZAN reduced the levels of the toxic peptide A42 by approximately 70%, by modulating the action of gamma-secretase.Flurizan reduces amyloid pathology in the brain and prevents memory defects in transgenic mice. ALZHEMEDNeurochem Inc.3Alzhemed is an oral small entire molecule that has been designed to interfere with the association between glycosaminoglycans (GAGs) and A amyloid protein. It is thus thought to prevent GAGs from promoting -sheet and amyloid formation.Designed to prevent amyloid formation and deposition in the brain, and thus modify the itinerary of AD. Alzhemed is expected to act on two levels firstly to prevent and stop the formation and deposition of amyloid fibrils in the brain as headspring as to bind to soluble A, and secondly to to inhibit the inflammatory response associated with amyloid build-up in AD.Inhibit A fibrillization and binds and reduces soluble A.VP025Vasogen1 liaise via the regulation of microglial cell activation.Treatment with VP025 relapsingd age-related decreases in CD200 levels in the brain, reduced levels of microglial cell activation, and restored memory and learning function.Considerable amount of preclinical work has demonstrated the ability of VP025 to reduce inflammation in models of a number of neurodegenerative diseases.the ability of VP025 to reverse detrimental neurological effects of chronic beta-amyloid exposurethe ability of VP025 to reverse age-related inflammation in the brainAAB-001Elan Pharmaceuticals, Inc., Wyeth.3Designed to bind and remove the A peptide that accumulates in the brain.Immunotherapy approaches to the treatment of Alzheimer disease is based on the ability of antibodies raised against A peptides to bind to and clear A from the brain, thus re wretched the peptide and inhibiting the damage to neurons that A inflicts.Anti-A antibodies have b een shown to prevent the accumulation of A peptides in the brains of transgenic mouse models of AD (Shenk et al., 1999 Bard et al., 2000 DeMattos et al., 2001).In one clinical trial, patients immunized with A peptide who actively generated anti-A antibodies showed a significantly slow-moving rate of decline in cognitive functions (Hock et al., 2003).Long-term follow-up studies of the patients who were involved in the failed phase 2a clinical trial of AN-1792 has shown that NTB (quality of life) scores remained significantly improved in antibody responders. In addition, CSF tau was significantly decreased in antibody responders (Gilman et al., 2005). mop up In on Alzheimers-Lastly, fresh drugs tender genuine hope for repealing the malady.Concluding test outcomes will be out, for a complete novel generation of drugs designed to assault the fundamental basis of Alzheimers diseasemedicines that propose, what one specialist calls legitimate, substantial, irrefutable hope for those with mild to moderate forms of the illness.Within three years, its nearly assured, well have disease-modifying drugs that fundamentally amend the nature of Alzheimers.From drugs which facilitate alleviation of merely the symptoms of the disease, we are now moving towards an era which will comprise of drugs that not only slow down the disease, but encompass the potential to wholly reverse it.Scientists are certain that one of the more than four dozen drugs now in human trials will succeed. One of the most hopeful of those, Flurizan, from Myriad Genetics, should complete its tests in the next 18 months.Exceedingly few drugs make it to Phase III clinical trials, the final stride before a drug goes to the FDA for authorization. Today, conversely, nine new Alzheimers treatments are in Phase III trials to test their effectiveness on a large number of patients. And dozens more are in smaller Phase II trials. This subsequent generation of drugs is deliberated to avert, obliterate and clean out d eposits of beta-amyloid plaque that exterminate the brains nerve cells, leading to the distressful loss of memory, reason and, eventually, life that typifies Alzheimers. This optimistic information comes as the world awaits an epidemic of Alzheimers, the traumatic transmutation of dementia that Americans tell pollsters they dread more than heart disease, stroke or diabetes. Today, 5.1 million people in the United States suffer from the disease, but the supreme risk factor is agethe longer a person lives, the greater the likelihoodand in just four years millions of boomers begin to turn 65. One in eight people age 65 and older now has Alzheimers half of those 85 and older have it. Connoisseurs say still if Alzhemed or another of these premature anti-amyloid drugs fails, that doesnt mean the amyloid theory is incorrect. It merely may mean that the drug didnt eliminate sufficient plaque to appreciably slow or arrest the disease. Finally, with the approach of such promising drugs into the market in the near future, there is potential to mitigate the humanity of the immoderate fiscal burden due to the disturbing tempo at which Alzheimers is making headway. Keeping our fingers cover might just help.References http//www.myriad.com/alzheimers/flurizan.phphttp//www.vasogen.com/sec/vp025http//www.alzforum.org/http//www.alz.org/national/documents/PR_FFfactsheet.pdfhttp//www.alz.org/national/documents/PR_FFquotesheet.pdfhttp//www.medicinenet.comhttp//www.pharmaceutical-business-review.comhttp//www.theracarb.com/documents/investor_%20presentation.pdfhttp //www.wikipedia.com