ALZHEIMER'S DISEASE.   Term Paper ID:28723 Click to get this paper

Essay Subject: Damage to brain cells caused by neurodegenerative disorder. Symptoms, diagnosis, progression of disease, theories re: causes, treatment, identifying risk factors.... More...

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Paper Abstract: Damage to brain cells caused by neurodegenerative disorder. Symptoms, diagnosis, progression of disease, theories re: causes, treatment, identifying risk factors. Paper Introduction: Alzheimer=s disease is a neurodegenerative disorder which causes the destruction of certain brain cells resulting in a decline in mental functions. The damage occurs in the association area of the cerebral cortex, the hippocampus and the middle and temporal lobes, and result in a decreased concentration of the neurotransmitter acetylcholine (Sadovsky, 2000, p. 877). Alzheimer=s disease affects the memory, thinking, language, and behavior. It usually occurs in people over the age of 65, but can occur in those as young as 40 years of age. Symptoms can range from mild to severe, and when dementia occurs, patients are often placed in full-time residential care. It is estimated that about 10 percent of the population over the age of 65 suffer from Alzheimer=s disease (Alzheimer=s, 1999). Of these, between five percent and 10 perce Text of the Paper: The entire text of the paper is shown below. However, the text is somewhat scrambled. We want to give you as much information as we possibly can about our papers and essays, but we cannot give them away for free. In the text below you will find that while disordered, many of the phrases are essentially intact. From this text you will be able to get a solid sense of the writing style, the concepts addressed, and the sources used in the research paper. of the cerebralcortex the hippocampus and the middle and but canoccur in those as young as age of suffer from Alzheimer s age Chemical and structural changes the disease The first symptoms are usually forgetfulness memory loss about him herself and others Personality and emotions actual diagnosis of Alzheimer s can only testing arecarried out If there is no other cause alteredmetabolism of beta-amyloid precursor protein APP and accumulation of the human rat or mouse APP to study mediated apoptosis occurring by binding induced by C These researchers Otherfeatures indicative of apoptosis were found the formation of caused by C Also priorincubation C mediated neuronal degeneration This C caused local neuritic degeneration that and illustrates a property of the neuropathology seen in familial strongcorrelation has been found between of normal peopleand Alzheimer s gene on chromosome andseparate mutations of transmembrane protein genes on of the Epsilon isoform of apolipoprotein E ApoE of A beta peptide specifically the fragmentthat is especially the pathogenesis of Alzheimer sdisease A presented at the conference that missense above It hasnow been found but is not necessary or angiotensin convertingenzyme antichymotrypsin bleomycin hydrolase butyrylcholinesterase HLA low density unknown at present Edwardson and has also suggested a susceptibility gene forAlzheimer s disease on wasperformed on the families presorted for the presence or all families butsignificant evidence for linkage Linkage analysis confirmed linkage tochromosome with the strongest s disease susceptibility genes on other chromosomes Individuals at of a geneallele associated with the disease and A prospective study is beingconducted on healthy bloodtests The participants will be cognitive tasks than the older ApoE-positive group didworse on a test for attention The amount their CSF comparedwith ApoE-negative at-risk nodifference between the at-risk group and the basis for the use ofcholinesterase inhibitors in their treatment Because fewer social activities and lower occupationalattainment limitedbeneficial effects and a poor effectprofile but requires more time for including cyclooxygenase inhibitors and steroids studies have demonstrated significant benefits for Alzheimer spatients who improvement in global changes in less overall decline than patients without vascular risk s Disease Assessment Scale during a one-yearperiod nicotine receptors in the brain Researchersbelieve that both actions in treating behaviordisturbances and patients on cholinesterase inhibitors appear to behavioral andpsychological signs although they often have separate neurochemical protecting against developingAlzheimer s later in life is working at of subjects studied at the University Hospitals ofCleveland all over age nearly percent of present great strides have been made indeveloping active may delay or prevent Alzheimer BMJ p Cheng G-S Biomarkers subtle number of genetic risk factors associated with the disorder isincreasing Fam Pract News p O Hara pp Rohn T T A monoclonal antibody to amyloid precursorprotein certain brain cells resulting in a decline in mentalfunctions The the memory thinking language and behavior placed in full-timeresidential care It is of thedisease That is they have a family information Symptoms of Alzheimer s vary Alzheimer s progresses the person becomes disoriented and confused and As brain function diminishes the ability to talk move of probable Alzheimer scan be is believed to occur due to the deathof et al Rohn used a monoclonal cleavage that were consistent with neurons or a syntheticpeptide APP that contains the epitope for the amino terminal end ofhuman but the neurons with the general capsase inhibitor N-benzyloxycarbonyl-Val-Ala-Asp o-methyl complete protection from the C of C It was also demonstrated thatselective application to compartmental a monoclonal antibody to APP initially death associated with Alzheimer sdisease Several extracellular plaquescontaining beta-amyloid dystrophic neurites activated microglia reactiveastrocytes the degree of dementia observedin life Beta-amyloid of genetic mutations have been found to early onset Alzheimer s before age and are inherited in have in common is that the density of A beta plaques all of whichindicate thatyear on the genetic basis for genetic factor indisputably linked with the lateonset forms single gene locus on chromosome ApoE can be usedto A whole string of genetic associations have been of these hasbeen systematically replicated in experiments so their familial Alzheimer s disease with earlyonset for appropriate disease Rogaeva A retrospectivecohort study of DNA data markers was found if familial Alzheimer s isassumed theAlzheimer s gene could not be determined but s diseasesusceptibility locus on chromosome cognitivedeficits Cheng Cognitively normal individuals with a familyhistory between this finding andactual development battery of tests for cognitive and biological markers including the disease Atbaseline testing the younger at-risk controls Individuals with and without ApoE performedsimilarly normal in both groups Individuals therest is being deposited in the difference in response tothe scopolamine challenge Alzheimer s factors include a family history of dementia female poor the duration of acetylcholine action atsynapses Tacrine the earliest scores with a better sideeffect profile A newer drug proof of its ability to reduce benefits inimproving cognition and delaying progression of Alzheimer s but in dailyliving behavior cognition memory self-care and overall receiving rivastigmine for weeks compared to controls who receivedplacebo Those with mild to moderate Alzheimer s diseaseshowed that those year of the test Galantamine is an associatedwith Alzheimer s is a major health care concern Ballard drowsiness tardive dyskinesia falls accelerated cognitive decline psychological signs in Alzheimer s age onwardscorrelated with a decreased risk of developing Alzheimer demands of the job or the subject s income of those with Alzheimer s While Alzheimer s remains a counseling and inproviding individuals with some means of Clin Ref Syst p Ballard C O p Edwardson J Morris C The sdisease Am Fam Phys p Moon E Evidence for an Alzheimer s diseasesusceptibility locus E Mantyh P W New insightsinto the neuropathology and Alzheimer s disease is a neurodegenerative temporal lobes and result in adecreased concentration of the years of age Symptoms can range from disease Alzheimer s Ofthese between in patients with Alzheimer s interferewith a person and difficultyunderstanding written material Alzheimer s Recent change and the patient may suffer from be made after death sinceit entails dissection for the symptoms then a diagnosisof Alzheimer of itsbeta-amyloid fragment are key features of Alzheimer s its role Exposure of cortical neurons to to APP since preincubation of also showed that mouse immunoglobulin G and kDa breakdown products of fodrin when cortical neurons of cortical neurons with GSH ethyl ester GEF was further supported by pre-treatment of the neurons with was prevented by the additionof GEF to the neuritic this protein in neurons that maycontribute and sporadic Alzheimer sdisease The hallmarks the amount of amyloid found in thebrains patients so it is not an abnormal protein chromosomes and identified as presenilin and presenilin significantly increases the risk of prone to aggregation ApoE appears to report in the British Medical Journal in summarized the datapresented mutations in threegenes causes autosomal dominant forms that three common allelic variants of ApoE exist e sufficient to causethe disease At most only half of lipoprotein receptor related protein various Morris The mutations in APP presenilin and presenilin chromosome after an analysis of such a link in absence of theApoE allele among affected members No evidence of was detected in the presence of locusheterogeneity using evidence at D S This providesindependent confirmation of risk for Alzheimer s disease have an increasedprevalence of certain have an abnormal level of beta-amyloid in the cognitively normal at-risk individuals with afamily history of Alzheimer s tested every five to years to see control group The at-risk group had asignificantly increased prevalence of spinal fluid tau protein which is found in neurofibrillary and control individuals Alzheimer s patientsusually have half as controls in behavioral changesor mood disturbances brain volumes by early intervention may prolong functioning in patients withAlzheimer s disease Sadovsky The main treatment for Alzheimer s is the side effect profile includinghepatotoxicity Donepezil is a highly selective dosage titration than donepezil Estrogen therapy increase acetylcholine are under investigation Antioxidants includingselegiline vitamin were at risk for developing vascular cognitiveabilities behavior and functioning as well as significant Another promising new drug is galantamine The scale measure memory language orientation and other aspectsof cognition lead to increased acetylcholine levels in thebrain Managing the have lesspsychotic symptoms Neuroleptic drugs are often used but these andneurophysiological bases No definitive treatment has a mentally demanding job Moon Working Alzheimer s Center The correlation held controlshad held jobs in managerial or screening tests for potential victims Although predictivefactors are not s alsoprovides hope for those considered at-risk for cognitive deficits flagincreased risk for steadily BMJ pp Kumar V R Update on Alzheimer s disease recent findingsand treatments induces neuronal apoptosis J Neurochem pp Voelker R Promising Alzheimer damage occurs in the association area It usually occurs in people over the age of estimated that about percent of the populationover the history of Alzheimer s and show signsof the disease before and change with progression of can no longer remembermajor facts or care for themselves is lost An made after a medical history physical exam and memory neuronal cells and there is considerable evidence that the antibody C which binds to theextracellular domain dying by apoptosis Thissupports a role for C for C significantlyattenuated neuronal damage not rat APP had no apparent effects on neuronal cells fluoromethyl ketone prevented boththe morphological and the biochemical changes destruction implicating an oxidative pathway in cultures of hippocampal neurons of triggers neuritedegeneration that is followed by capsase-dependent apoptosis in neuronalcultures lines of evidence suggest that beta-amyloid is directlyinvolved in and neuronal loss Weldon Maggio and Mantyh A is found in the cerebrospinal fluid be associatedwith Alzheimer s disease mutations of the APP an autosomal dominant fashion Also polymorphism they all appear toincrease the productions a central role for A beta in Alzheimer s Edwardson and Morris Evidence was of Alzheimer s that is the ApoE also described predict risk of Alzheimer s reported with lateonset Alzheimer s including polymorphisms in significance inrelation to Alzheimer s is genetic counseling and support A recent study for six chromosome genetic markers to arise from the same genetic locus in includes the entire regionsuggested by earlier studies and suggests the existence ofAlzheimer of Alzheimer s disease have an increased prevalence of Alzheimer s is unknown genetic testing spinal fluid analysis brain imaging and group performed slightly worse onmost overall in cognitive testing but the who were ApoE-positive had markedly lower levels of beta-amyloid in brain in these patients There was patients have a markedly increasedsensitivity to scopolamine providing the nutrition atherosclerotic vascular disease head injury depression engaging in drug in this group has only rivastigmine has a good side the risk of Alzheimer sdisease is inconclusive Anti-inflammatory drugs outcomeshave been variable making treatment recommendations difficult Threeprospective diseaseseverity Patients with and without vascular risk factors demonstratedstatistically significant patients with vascular risk receiving rivastigminedemonstrated treated with galantamine maintained or improved theirscores on the Alzheimer acetylcholinesterase inhibitor and also appears to act on and O Brien Risperidone has been found to be beneficial and severe neuroleptic sensitivityreactions Clinical trials often lump together disease One thing which has been found useful in s in a case-controlled study educationalattainment and childhood socioeconomic status Analyzing Alzheimer spatients and controls severely debilitating ailment and littletreatment is available at preparing for the future Thefinding that staying mentally Brien J Treating behavioral andpsychological signs in Alzheimer s disease genetics of Alzheimer sdisease the M A Mentally demanding work may deter Alzheimer sdisease on chromosome and for further locus heterogeneity JAMA cell biology of Alzheimer s disease Geriatrics pp disorder which causes thedestruction of neurotransmitter acetylcholine Sadovsky p Alzheimer s disease affects mildto severe and when dementia occurs patients are often five percent and percent have the familial form s ability to process store and retrieve memory isaffected more severely than longterm memory As delusions hallucinations anxiety andloss of motivation of the brain A diagnosis s is made Alzheimer s disease However the normal function of APP is unknown Rohn C induced morphological changesincluding neurite degeneration nuclear condensation and internucleosomalDNA C with either purified APP and themonoclonal antibody P which is specific were treated with C but pretreatment of a cell-permeableform of GSH resulted in buthioninesulfoximine an inhibitor of gamma-glutamylcysteinyl synthetase potentiated the toxic effects compartment Overall the results showed that thebinding of to the profound neuronal cell of Alzheimer s pathology are of Alzheimer s patients at death and specific toAlzheimer s only its accumulation is Three groups respectively Weldon Maggioand Mantyh These mutations contribute to both familial and sporadic Alzheimer s The feature these mutations increase both thedeposition of A beta and at the th International Conference on Alzheimer s disease of early onset Alzheimer s asdescribed above and one e and e encoded as a late onset Alzheimer s patients carryan ApoE allele mitochondrialenzymes and the presenilin intronic mutation So far none allow for geneticscreening in suspected cases of families with a history of the linkage to the regionspanned by the chromosome the admixture test The precise location of the existence of an Alzheimer biological markers and may have subtle spinal fluid but the relationship and controls with no family history Theyhave been given a ifpositive markers are associated with development of of ApoE percent compare to percent in the tangles and is twice as abundant inAlzheimer s patients was much ApoE in their spinal fluid and it is thought magnetic resonance imaging ororthostatic blood pressure Also there was no identifying risk factors has become important Commonly identified risk use of anticholinesteraseinhibitors which increase acetylcholinesteraseinhibitor that significantly improves cognitive concentrations and has antioxidantactivity but E and Ginkgo biloba have demonstrated some dementia withrivastigmine tartrate Kumar Improvement was noted clinicallymeaningful improvements in ability to perform activities of daily livingafter Voelker Amulticenter study of patients The patients also maintained activities of daily living forthe behavioral and psychological signs of dementia have manyside effects including parkinsonism yet emerged for thebehavioral and at a mentally challenging occupation from true regardless of thesocial and physical professional specialties that were mentallydemanding compared with only percent absolute they are important for genetic the disease References Alzheimer s Disease November Alzheimer s Fam Pract News New treatment for patients with Alzheimer West J Med pp Rogaeva s drug JAMA p Weldon D T Maggio J of the cerebralcortex the hippocampus and the middle and but canoccur in those as young as age of suffer from Alzheimer s age Chemical and structural changes the disease The first symptoms are usually forgetfulness memory loss about him herself and others Personality and emotions actual diagnosis of Alzheimer s can only testing arecarried out If there is no other cause alteredmetabolism of beta-amyloid precursor protein APP and accumulation of the human rat or mouse APP to study mediated apoptosis occurring by binding induced by C These researchers Otherfeatures indicative of apoptosis were found the formation of caused by C Also priorincubation C mediated neuronal degeneration This C caused local neuritic degeneration that and illustrates a property of the neuropathology seen in familial strongcorrelation has been found between of normal peopleand Alzheimer s gene on chromosome andseparate mutations of transmembrane protein genes on of the Epsilon isoform of apolipoprotein E ApoE of A beta peptide specifically the fragmentthat is especially the pathogenesis of Alzheimer sdisease A presented at the conference that missense above It hasnow been found but is not necessary or angiotensin convertingenzyme antichymotrypsin bleomycin hydrolase butyrylcholinesterase HLA low density unknown at present Edwardson and has also suggested a susceptibility gene forAlzheimer s disease on wasperformed on the families presorted for the presence or all families butsignificant evidence for linkage Linkage analysis confirmed linkage tochromosome with the strongest s disease susceptibility genes on other chromosomes Individuals at of a geneallele associated with the disease and A prospective study is beingconducted on healthy bloodtests The participants will be cognitive tasks than the older ApoE-positive group didworse on a test for attention The amount their CSF comparedwith ApoE-negative at-risk nodifference between the at-risk group and the basis for the use ofcholinesterase inhibitors in their treatment Because fewer social activities and lower occupationalattainment limitedbeneficial effects and a poor effectprofile but requires more time for including cyclooxygenase inhibitors and steroids studies have demonstrated significant benefits for Alzheimer spatients who improvement in global changes in less overall decline than patients without vascular risk s Disease Assessment Scale during a one-yearperiod nicotine receptors in the brain Researchersbelieve that both actions in treating behaviordisturbances and patients on cholinesterase inhibitors appear to behavioral andpsychological signs although they often have separate neurochemical protecting against developingAlzheimer s later in life is working at of subjects studied at the University Hospitals ofCleveland all over age nearly percent of present great strides have been made indeveloping active may delay or prevent Alzheimer BMJ p Cheng G-S Biomarkers subtle number of genetic risk factors associated with the disorder isincreasing Fam Pract News p O Hara pp Rohn T T A monoclonal antibody to amyloid precursorprotein certain brain cells resulting in a decline in mentalfunctions The the memory thinking language and behavior placed in full-timeresidential care It is of thedisease That is they have a family information Symptoms of Alzheimer s vary Alzheimer s progresses the person becomes disoriented and confused and As brain function diminishes the ability to talk move of probable Alzheimer scan be is believed to occur due to the deathof et al Rohn used a monoclonal cleavage that were consistent with neurons or a syntheticpeptide APP that contains the epitope for the amino terminal end ofhuman but the neurons with the general capsase inhibitor N-benzyloxycarbonyl-Val-Ala-Asp o-methyl complete protection from the C of C It was also demonstrated thatselective application to compartmental a monoclonal antibody to APP initially death associated with Alzheimer sdisease Several extracellular plaquescontaining beta-amyloid dystrophic neurites activated microglia reactiveastrocytes the degree of dementia observedin life Beta-amyloid of genetic mutations have been found to early onset Alzheimer s before age and are inherited in have in common is that the density of A beta plaques all of whichindicate thatyear on the genetic basis for genetic factor indisputably linked with the lateonset forms single gene locus on chromosome ApoE can be usedto A whole string of genetic associations have been of these hasbeen systematically replicated in experiments so their familial Alzheimer s disease with earlyonset for appropriate disease Rogaeva A retrospectivecohort study of DNA data markers was found if familial Alzheimer s isassumed theAlzheimer s gene could not be determined but s diseasesusceptibility locus on chromosome cognitivedeficits Cheng Cognitively normal individuals with a familyhistory between this finding andactual development battery of tests for cognitive and biological markers including the disease Atbaseline testing the younger at-risk controls Individuals with and without ApoE performedsimilarly normal in both groups Individuals therest is being deposited in the difference in response tothe scopolamine challenge Alzheimer s factors include a family history of dementia female poor the duration of acetylcholine action atsynapses Tacrine the earliest scores with a better sideeffect profile A newer drug proof of its ability to reduce benefits inimproving cognition and delaying progression of Alzheimer s but in dailyliving behavior cognition memory self-care and overall receiving rivastigmine for weeks compared to controls who receivedplacebo Those with mild to moderate Alzheimer s diseaseshowed that those year of the test Galantamine is an associatedwith Alzheimer s is a major health care concern Ballard drowsiness tardive dyskinesia falls accelerated cognitive decline psychological signs in Alzheimer s age onwardscorrelated with a decreased risk of developing Alzheimer demands of the job or the subject s income of those with Alzheimer s While Alzheimer s remains a counseling and inproviding individuals with some means of Clin Ref Syst p Ballard C O p Edwardson J Morris C The sdisease Am Fam Phys p Moon E Evidence for an Alzheimer s diseasesusceptibility locus E Mantyh P W New insightsinto the neuropathology and If this paper is not what you are looking for, you can search again: Search for: or Click here to request an essay written just for you.