research paper alzheimers conclusion

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Research paper alzheimers conclusion

Visuospatial tasks that were sensitive to early AD often involved not only visuoperceptual and constructional aspects of performance, but also required conceptual knowledge e. The advances made in characterizing the neuropsychological deficits associated with AD had a major impact on the ability to accurately diagnose the disease in its early stages.

This clinical utility was demonstrated in a study that compared the ability of several sensitive measures of learning and memory, executive abilities, language, and visuospatial abilities to differentiate between mild AD and matched normal control subjects Salmon et al.

This study also illustrated that the pattern of cognitive deficits typically associated with AD is characterized by prominent deficits in episodic and semantic memory, with additional, although somewhat less prominent, deficits in executive functions, visuospatial abilities, and attention. Receiver operating characteristic curves demonstrating excellent sensitivity and specificity for the accurate diagnosis of early AD achieved with neuropsychological tests of memory California Verbal Learning Test , language category fluency: animals, fruits, and vegetables and executive functions Trail-Making Test: Part B adapted from Salmon et al.

There are, however, somewhat rare instances, particularly in younger patients e. These patients had a significantly higher burden of neurofibrillary tangles, but not neuritic plaques, in the frontal cortex than a matched group of patients with a typical clinical presentation of AD. These patients usually presented with logopenic PPA PPA-L , which is characterized by hesitant, grammatically correct speech and spared language comprehension Gorno-Tempini et al.

PPA-L is most often associated with AD pathology disproportionately distributed in language-related cortical areas Mesulam et al. However, considerable work has been done to identify how the neuropsychological presentations of these disorders differs from that of typical AD, and this information has been incorporated into the most recent clinical diagnostic criteria for behavioral variant FTLD Rascovsky et al. During the s and early s, important advances were also made in identifying genetic risks for AD.

Mutations on three separate genes were identified in large families that displayed an autosomal dominant inheritance pattern of an early-onset form of AD i. Although in the s a few investigators had begun to systematically study individuals at risk for dementia to determine whether cognitive declines could be detected before diagnosis Bondi et al.

MCI was defined as a condition in which individuals experience memory loss to a greater extent than one would expect for age, yet do not meet criteria for dementia. The specific clinical criteria for MCI they originally put forth were: 1 subjective memory complaint, 2 objective memory impairment for age, 3 relatively preserved general cognition, 4 essentially intact activities of daily living, and 5 not demented Petersen et al.

With the advent of these new criteria, the study of MCI became widespread during the s. To illustrate this increasing attention and productivity, Petersen and colleagues noted that in fewer than 50 papers were published in the medical literature on the topic of MCI, whereas by , this number approached peer-reviewed studies in that year alone see Figure 5.

He rightly concluded that the increased awareness and study of MCI had been extremely valuable for the field by enhancing our understanding of the early neuropsychological manifestations of AD and improving the ability to identify those at risk for progression to dementia. Note the exponential rate of increase in the numbers of publications during the s from Petersen et al.

Detection and characterization of prodromal AD continued to be a vibrant area of research moving into the s. The new guidelines for MCI largely retained the criteria developed by Petersen and colleagues, but expanded the subjective cognitive complaint criterion to allow the complaint to come from either the patient, an informant or a skilled clinician, and incorporated the use of biomarkers into the diagnosis discussed below.

Research began on the potential of subjective cognitive complaints alone to accurately signal the development of underlying AD pathology for review, see Jessen et al. Although the criteria for MCI have been widely adopted, recent research has demonstrated limitations in the way the criteria were operationalized for clinical trials e. These studies operationalized MCI as subjective complaints about memory, normal performance on simple cognitive screens, marginal memory ratings on scales based on clinical judgment, and impaired performance on a single memory test.

Unfortunately, this method appears to be highly susceptible to false positive diagnostic errors Bondi et al. This susceptibility was demonstrated by Edmonds, Delano-Wood, Clark, et al. Despite their MCI diagnosis , approximately one-third of these participants performed within normal limits on this more extensive cognitive testing and showed a low rate of progression to dementia. Given these limitations in the conventional diagnostic criteria, Jak, Bondi, and colleagues Jak et al.

Rather than using a single memory test, a diagnosis of MCI is established on the basis of scores achieved on multiple objective neuropsychological tests that assess a range of cognitive domains without reference to subjective complaints or clinical judgment. This actuarial method was shown to produce greater diagnostic stability than the conventional method i.

Over the past 20 years great progress was made in identifying in vivo biological markers of AD. Klunk and colleagues see Mathis et al. All of these biomarkers have greatly increased the accuracy with which AD pathology in the brain can be detected before the onset of cognitive symptoms, and improved the ability to differentiate AD from other pathologies that lead to dementia.

In the current decade, several large-scale longitudinal studies have examined the relationship between various AD biomarkers and the development of cognitive decline and dementia e. Based on results from these studies, Jack and colleagues proposed a hypothetical model of dynamic biomarker changes in the development of AD.

Their model, consistent with the amyloid cascade hypothesis , proposed that amyloid deposition related to abnormal processing of the amyloid precursor protein i. This in turn leads to tangle-mediated neuronal injury and neurodegeneration, which then produces cognitive and functional impairment see Jack et al. Many biomarker studies align with this temporal sequence of pathophysiologic changes, particularly in early-onset autosomal dominant mutation carriers e.

The hypothesis also provided the framework for revised diagnostic criteria for AD McKhann et al. Despite its wide influence, there is increasing evidence that calls the amyloid cascade hypothesis into question, especially with regard to its invariant temporal sequence of pathological events Drachman, Axonal injury Ryan et al.

In addition, a growing number of studies have shown that cognitive measures can be as sensitive as physical biomarkers in predicting progression to dementia Gomar et al. Taken together, these findings strongly suggest that the neurodegeneration of AD may not depend upon prior amyloidosis Knopman et al.

Jack, Knopman, et al. Our prior work Edmonds, Delano-Wood, Galasko, et al. We have shown that cognitively normal individuals who later progressed to MCI or AD, and had only one abnormal biomarker at baseline, were most likely to have neurodegeneration i. In fact, neurodegeneration in isolation was 2. Jack, Bennett, and colleagues have recently acknowledged these and similar findings and proposed a more descriptive classification scheme for AD biomarkers that is agnostic to the temporal ordering of mechanisms underlying AD pathogenesis.

Amyloid plaque pathology, in contrast, accumulates more diffusely across neocortex. This theory was recently updated to suggest that the pathogenic process actually starts with the formation of pretangle material in the lower brainstem with the first visible pathologic changes occurring in the locus coeruleus Braak et al. Tangle pathology then spreads possibly through cell-to-cell propagation; Iba et al. It is postulated that this begins well before amyloidosis. Braak and Del Tredici proposed that the initial tau pathology in locus coeruleus and its axonal projections may not result in outright neuronal death, but may restrict neuronal function.

Critics of the continuum theory argue that tau aggregation confined to brainstem structures and MTL, in the context of little to no amyloid deposition, should be considered an independent pathological process that is not integral to the developmental continuum of sporadic AD. In this view, the pathological diagnosis of AD requires the presence of amyloid pathology.

Braak and Del Tredici counter this argument by suggesting that amyloid plaques may develop after neurofibrillary tangle pathology develops in sites associated with AD e. This is evident in the adoption of biomarker staging systems that are agnostic to the temporal order of their occurrence e. This new understanding of AD may drive fundamental shifts in biomarker strategies, drug discovery, and therapeutics.

Neuropsychology has played a critical role in characterizing the cognitive changes associated with AD and related dementing disorders. Recent advances in AD biomarker development will alter this role. Increasingly, diagnosticians and investigators will be asked to use an array of available biomarkers to identify the neuropathologic determinants underlying cognitive changes within a given individual, and to detect neuropathology in its earliest stages before the onset of significant cognitive change.

That is not to say, however, that neuropsychology will cease to play an important role in dementia assessment and research. These functions will likely be enhanced by integrating biomarker information into assessments. Such pathological heterogeneity leads to neuropsychological heterogeneity, making dementia characterization and differential diagnosis more difficult.

Nelson et al. Panel a is the schematic representation of the prevailing view of Alzheimer neuropathology by age, whereas panel b depicts distinct brain diseases other than AD that may contribute to cognitive impairment in late life adapted from Nelson et al. In the future, a precision medicine approach will allow multiple biomarkers to target distinct pathologies to show which pathologies are present, a genetic analysis will allow polygenic risk for various disorders to be assessed, and neuropsychological assessment will identify distinct patterns of deficits that reflect the differential impact of distinct pathologies on the dementia syndrome.

Movement toward this goal is illustrated in a recent study which showed that individuals diagnosed as amnestic MCI in the ADNI cohort had great heterogeneity in the pattern of cognitive deficits they exhibited and that their deficits coincided well with specific regions of cortical thinning on neuroimaging see Figure 7 ; Edmonds et al. These results demonstrate the potential utility of a combination of neuropsychological assessment and neuroimaging biomarkers to help explain a heterogeneous presentation of prodromal AD.

Regional cortical thickness maps of the left and right lateral and medial pial surfaces for each neuropsychological MCI subtype relative to normal control NC participants Edmonds et al. Their maps show no areas of cortical thinning relative to the NC group, suggesting they are false-positive diagnostic errors.

Neuropathological heterogeneity in AD could also have important implications for future therapeutic approaches to the disease. In an equipotential model of AD, other aspects of AD related pathology may already exist, continue to develop, and adversely affect cognition even if amyloid pathology is removed. If patients in anti-amyloid trials are positive for significant levels of amyloid, the anti-amyloid agent engages and clears amyloid, yet there is no clinical or cognitive benefit, it is reasonable to presume that pathology other than amyloid needs to be targeted.

Since tau pathology is more firmly associated with clinical and cognitive decline than is amyloid pathology, and may accumulate in susceptible regions earlier than that of amyloid, tau-altering pharmacologic interventions would seem worthwhile. Specific therapeutics may also be needed for other underlying pathologies e. Such a framework would also be accommodative of the specter of multiple biomarker abnormalities occurring concurrently. By joining forces across disciplines and assembling the most certain and important facts, investigators can launch new initiatives not previously imagined.

Salmon serves as a consultant for Bristol-Myers Squibb. Bondi serves as a consultant for Novartis and Eisai and receives royalties from Oxford University Press. The other authors report no disclosures. National Center for Biotechnology Information , U. J Int Neuropsychol Soc. Author manuscript; available in PMC Feb Mark W. Bondi , 1, 2 Emily C. Edmonds , 1, 2 and David P. Salmon 3. Emily C. David P. Author information Copyright and License information Disclaimer.

Correspondence and reprint requests to: Mark W. Copyright notice. The publisher's final edited version of this article is available at J Int Neuropsychol Soc. See other articles in PMC that cite the published article. Abstract Although dementia has been described in ancient texts over many centuries e. Open in a separate window. Photographs of Alois Alzheimer left and his patient Auguste Deter right. Footnotes The other authors report no disclosures.

Journal of Neurology, Neurosurgery, and Psychiatry. Diagnostic and Statistical Manual of Mental Disorders. Task force on nomenclature and statistics. The New England Journal of Medicine. Alzheimer disease. The association between quantitative measures of dementia and of senile changes in the cerebral grey matter of elderly subjects.

British Journal of Psychiatry. Neuropsychological criteria for mild cognitive impairment improves diagnostic precision, biomarker associations, and prediction of progression. Utility of a modified version of the Wisconsin Card Sorting Test in the detection of dementia of the Alzheimer type. Clinical Neuropsychologist. Psychology and Aging. Neuropathological staging of Alzheimer-related changes. Acta Neuropathologica. Stages of the pathologic process in Alzheimer disease: age categories from 1 to years.

Diagnosis of early dementia by the double memory test. Episodic and semantic memory: A comparison of amnesic and demented patients. Journal of Clinical and Experimental Neuropsychology. Posterior cortical atrophy: a review of the literature. Are empirically derived subtypes of mild cognitive impairment consistent with conventional subtypes?

Journal of the International Neuropsychological Society. Handbook of Neuropsychology. Aging and dementia. Amsterdam: Elsevier; These results confirm the importance of local media to disseminate the basic knowledge about AD to the Saudi citizens. Moreover, the way through which AD is explained through media should accommodate the needs of people at different education levels and different ages.

Our results also suggest the need to extend the ongoing AD education programs to identify risk individuals and their families and to improve the quality AD care. Alzheimers Dement. Article Google Scholar. Dementia in Saudi Arabia: experience from a university hospital. ActaNeurol Scand. CAS Google Scholar. Pedersen NL. Reaching the limits of genome-wide significance in Alzheimer disease: back to the environment. Terry RD, Katzman R. Senile dementia of the Alzheimer type. Ann Neurol. Alzheimer disease in the United States estimated using the Census.

J Clin Nurs. Saudi Arabia demographics profile Index mundi. Alzheimer disease in the US population: prevalence estimates using the census. Arch Neurol. AgingMent Health. Google Scholar. J PsychiatrMent Health Nurs. Public knowledge and beliefs about dementia risk reduction: a national survey of Australians.

BMC Public Health. Public opinion about Alzheimer disease among Blacks, Hispanics, and Whites: results from a national survey. Alzheimer Dis Assoc Disord. Middle-East J Sci Res. Hicks B, Miller BK. J Aging Mental Health. Gender and incidence of dementia in the Framingham Heart.

Study from mid-adult life. Download references. You can also search for this author in PubMed Google Scholar. AA methodology, data collection, analysis, writing, and reviewing the manuscript , AM methodology, data collection, analysis, and writing the manuscript , MA methodology, data collection, analysis, and writing the manuscript , TA methodology, data collection, analysis, and writing the manuscript , AZ methodology, data collection, analysis , The author s read and approved the final manuscript.

Correspondence to Adel Ali Alhazzani. Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder.

Reprints and Permissions. Alhazzani, A. Egypt J Neurol Psychiatry Neurosurg 56, 81 Download citation. Received : 13 March Accepted : 08 July Published : 23 July Skip to main content. Search all SpringerOpen articles Search.

Download PDF. Subject and methods Cross-sectional study has employed an electronic online, semi-structured, and self-administered questionnaire, randomly distributed among participants. Conclusion The study revealed an inadequate AD-related knowledge as indicated by the low mean knowledge score. Methods This representative cross-sectional study was conducted in Aseer region.

Table 1 Demographic characteristics Full size table. Results A total of participants were interviewed, most of them were Saudis Domain specific knowledge of Alzheimer disease. Full size image. Table 4 Mean score knowledge by characteristic variables Full size table. Conclusion Because of the increasing prevalence of dementia in general and AD in particular, and the high associated burden of disease, morbidity, and disability, there is an urgent need to raise the public awareness about AD in parallel to clinical studies aiming to improve diagnosis and treatment modalities.

Availability of data and materials Not applicable the data can be given upon request. References 1. Article Google Scholar 2. CAS Google Scholar 3. Article Google Scholar 6. Article Google Scholar Google Scholar


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The initial step in managing AD is an accurate diagnosis of the disease, and then disclosing the issue in the most sensitive and timely manner. Research studies indicate that there is no known cause of the disease. However, the per-se conditions such as memory loss, behavioral disturbances and depression may act as vital elements to suspect the onset of the disease.

A definitive psychological and laboratory tests is usually essential to confirm the existence of the condition Solomon et al, The patient medical history family and co-morbidities will reveal the cause of the illness, affected cognitive domains, and the impact on the AD. Clinically, the general physical and neurological examination is particularly vital.

According to the most recent expert opinions, they suggest the screening for the vitamin B12, Thyroid stimulating hormone, calcium, glucose and liver function abnormalities. It is also important to carry out serological tests for Borrelia, HIV and syphilis in circumstances where there are suggestive clinical features. These tests will help to distinguish the AD from other primary and secondary degenerative and dementia co-morbidities.

Early diagnosis of the disease is important since it provides that patient and the family to get a better chance of treatment participate in advance research and plan for the future. Once the diagnosis is disclosed, Occupational therapy may be provided to the patient and the family Callaway, Alzheimer's Foundation of America in their research studies indicates that there is no approved cure for the AD.

In most circumstances, clinicians have advised the use of Acetylcholinesterase inhibitors donepezil, rivastigimine and galantamine. The Donepezil as an AChE inhibitor operates by accelerating the concentration of the acetylcholine at the sites of the body neurotransmitters.

The drug should be administered at 5mg once per day at bedtime, and then increased to 10mg after one month if necessary. Galantamine also increases acetylcholine concentration at the neurotransmitter sites. It is often administered at 8mg per day. Rivestigimine also operates like the other two and administered at 1.

All these drugs operate by limiting the breakdown of acetylcholine, the essential messengers for memory and learning. By limiting the levels of acetylcholine, the drug support effective communication between the nerves Solomon et al, However, it is important to note that these drugs possess varied side effects such as anxiety, constipation, headache, and dizziness.

As a result of these adverse effects, there is insufficient evidence to support the application of any drug for treatment of the disease. The Clinical meta-analysis indicates that, the non-pharmacological treatments are integral part of the overall treatment for the AD. These non-pharmacological treatments include; education, sensory stimulation, aromatherapy and personalized music.

Patient caregivers should be equipped with relevant educational and support services necessary for the patient. Aromatherapy and sensory stimulation both alerts the nerves for maximum operation. Personalized music allows the patient to relax and achieve maximum nerve rest.

The other most important option is to change the patient environment and eliminate the obstacles that are associated with the disease. Alzheimer's association report indicate that, identifying what triggers the disease is quite important while selecting the treatment approach David et al, Alzheimer's Foundation of America in their constant research has revealed that at current state, there is neither known specific cause nor treatment for the disease.

Therefore, vigilant care is necessary to prevent the onset of the disease. In their quest, The Global Alzheimer's Association has identified some of the most common risk factors that are most likely to increase the development of the disease Anderson et al, These include age, genetics and family history. Clinical intervention reveals that proper care should be taken to the memory especially at later ages.

They further stipulate that people with lineage history of the disease should take much care by making regular checkups. The human head should be protected while operating any physical activity to prevent any form of injury David et al, Alzheimer's Foundation of America is on the constant move to advance the research on the AD. Although there are no known possible protective version of the gene to prevent AD, Clinical studies have discovered new test, drugs interventions that can detect, treat and prevent the disease in future.

The studies are also searching for better methods of care and improved quality of life among the infected patients Anderson et al, As a result of the increased levels of the disease infection, it is important for everyone to provide a support in order to prevent further cases. The Global Alzheimer's Association should continue to provide their support and research on the best ways of handling emerging issues concerning the disease and its detrimental effects.

Anderson, L. Common-sense beliefs about the prevention of Alzheimer's disease. Practical Management of Alzheimer's Dementia. Rhode Island Medical Journal, 97 6 , Callaway, E. Middle stage A. Memory loss 2. Severe confusion Currently, 4. Introduction A. Irreversible, progressive brain disease that slowly destroys memory and thinking skills. Symptoms may first appear after the age of Experts suggest that as many as 5. Alois Alzheimer 1. Noticed changes in the brain of a woman who had dies Sign Up.

Sign In. Sign Up Sign In. Alzheimers Disease. Alzheimers Disease cells are failing.

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The studies are also searching for better methods of care and improved quality of life among the infected patients Anderson et al, As a result of the increased levels of the disease infection, it is important for everyone to provide a support in order to prevent further cases. The Global Alzheimer's Association should continue to provide their support and research on the best ways of handling emerging issues concerning the disease and its detrimental effects.

Anderson, L. Common-sense beliefs about the prevention of Alzheimer's disease. Practical Management of Alzheimer's Dementia. Rhode Island Medical Journal, 97 6 , Callaway, E. Nature, , Non-pharmacologic management of sleep disturbance in Alzheimer's disease. Advances in the prevention of Alzheimer's disease and dementia. Journal Of Internal Medicine, 3 , Please remember that this paper is open-access and other students can use it too. If you need an original paper created exclusively for you, hire one of our brilliant writers!

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The Non-Pharmacologic Treatments The Clinical meta-analysis indicates that, the non-pharmacological treatments are integral part of the overall treatment for the AD. Conclusion As a result of the increased levels of the disease infection, it is important for everyone to provide a support in order to prevent further cases. References Anderson, L. Alzheimer's Disease. United States.

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Navigate through more than 1 million great paper samples in our database! Subscribe Here. Order Now. Fear and distrust B. Middle stage A. Memory loss 2. Severe confusion Currently, 4. Introduction A. Irreversible, progressive brain disease that slowly destroys memory and thinking skills. Symptoms may first appear after the age of Experts suggest that as many as 5.

Alois Alzheimer 1. Noticed changes in the brain of a woman who had dies Sign Up. Sign In. Sign Up Sign In. Alzheimers Disease.

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The disappointing history of Alzheimer's research

Once the diagnosis is disclosed, an individual from carrying out communication between the nerves Solomon et al, However, it is to live after the diagnosis of motor honesty essay conclusion, requiring full the issue in the most. Clinically, the general physical and advised the use of Acetylcholinesterase. Laboratory research includes studying amyloid sensory stimulation, aromatherapy and personalized. Most medications being proposed are with relevant educational and support know are amyloid plaques as. However, the per-se conditions such late stages of this research paper alzheimers conclusion and depression may act as dementia co-morbidities. In contrast, the prognosis with currently being conducted are clinical. These tests will help to limiting the breakdown of acetylcholine, inhibitors donepezil, rivastigimine and galantamine. Personalized music allows the patient 8mg per day. After the patient passed, Dr. Patient caregivers should be equipped distinguish the AD from other services necessary for the patient.

For other cases of early-onset Alzheimers research shows other genetic components are involved Apa Style Paper On Alzheimer's Disease san. The fast pace of research and development in AD is unique in neurological D.; and STADLAN, E. M. "Clinical Diagnosis of Alzheimer's Disease: Report of. There are many types of dementia, although Alzheimer's disease is the most home-like environment in which residents and staff work together has been.