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Alzheimer's Disease - Research, Effects, Evaluation, Approaches, and Treatment Methods

Updated on July 15, 2017

Cognition and Perception

“About 60% of elderly people with dementia have Alzheimer’s disease. Another percentage have what is called mixed dementia. Alzheimer’s and vascular dementia combined. Alzheimer’s disease attacks our humanity at its core. In this illness that has become a synonym for any dementia of old age, the neurons wither away” (Belsky, 1999, p. 213). Alzheimer’s does not just affect people during old age, “younger-onset (known as early-onset) Alzheimer’s affects people younger than age 65. Up to 5% of the more than 5 million Americans with Alzheimer’s have younger-onset. Many individuals with early onset are in their 40s and 50s. In the United States, it is estimated that approximately 200,000 people have early onset” (Alzheimer’s Association, 2016, para. 1-2). There is a lot of information available about Alzheimer’s disease, but a lot of learning about this horrible life-ending disease is needed as quickly as possible. Through scholarly research, this research paper provides information about the detrimental effects that Alzheimer’s disease has on a person’s memory, historical evaluations and approaches to the disorder, possible causes and treatments, and comparisons to current research regarding possible causes and treatments.

I. Effects on Memory

A. Even during the beginning stages of Alzheimer’s, a person’s memory is already being affected. For example, your grandmother may have lived in a certain area all of her life and driven to and from the local shopping center throughout her adult years. Then, one day, she drives out to the shopping center and she doesn’t recognize any of the shops, parking lot, or surrounding area. She has become confused by this, and now, she realizes that she does not know her way back home. This is an example of the beginning effects of Alzheimer’s disease, which is the most devastating type of dementia that exists. From here, her memory will become even more affected until she no longer recognizes close family members or the fact that she saw you just a few minutes earlier. (Belsky, 1999)

B. Shortages in working memory, a limited framework that helps the workings of the online control and transitory stockpiling of data are thought to be a sign of Alzheimer's disease (AD), even during its initial stage. Deficiencies in traverse errands and double assignment systems rise in the early phases of AD and have been ascribed to focal decision-making dysfunction. Specially noteworthy is the finding that people who are deemed to be at a higher risk for developing AD due to hereditary show poor working memory execution in comparison to those who are not at hereditary danger. Thus, enabling the capability of such assignments to enable initial AD. (Charlesworth, Allen, Morson, Burn, & Souchay, 2014, p. 1)

II. Historical Evaluations

A. Alzheimer’s disease is the most prevalent type of dementia that exists in the western countries. When being diagnosed with AD, it is mostly due to criteria of a clinical and historical nature. Much research has found that there is a pretty high degree of accuracy in diagnosing AD – at about 80% to 90%. These studies are normally conducted in centers that are specialized in the area of AD and this is normally conducted on people who were in the advanced stages of the disease. Presently, examinations that are conducted post-mortem are the only true way to determine the presence of AD. “The diagnosis of Alzheimer's disease (AD), the most common form of dementia in western countries, is largely based on historical and clinical criteria. For these reasons, developing a biomarker for this disease would be very beneficial for the successful diagnosis of Alzheimer’s disease. This biomarker could also be very beneficial for an effective measure in upcoming studies. (Ladenson, Laterza, & Modur, 2013, para. 4)

B. This audit concentrates on six key papers distributed in mid-2000 in light of work directed in Cambridge. The initial two identify with clinical-neurotic studies which built up that Alzheimer's infection (AD) is a moderately normal reason for central cortical disorders, eminently dynamic aphasia (to a great extent non-familiar), dynamic apraxia, and back cortical decay with complex visual manifestations. Expanding on these discoveries, criteria for the dynamic aphasias have been produced which characterize the variation connected with AD (dynamic logogenic aphasia). Memory in the dementias has been a noteworthy range of interest and one paper talked about here investigated the neural premise for long winded and semantic memory disappointment in AD and semantic dementia. Regardless of altogether different memory profiles, the two issue … cause serious hippocampal hypo-digestion system and decay however contrast in the level of contribution of other memory related structures. This work attracted consideration regarding the part of pathology in non-hippocampal structures ahead of schedule in AD. The following two articles manage the behavioral variation frontotemporal dementia (by FTD) which we have indicated is connected with a breakdown in the principle of the brain, social thinking, sympathy, and feeling preparing and added to take a shot at the neural premise of social comprehension. We additionally recognized a subgroup of by FTD who neglect to advance over numerous years, termed phenology cases, who are separated by their absence of decay on MRI. The last paper portrayed the utilization of the Addenbrooke's Cognitive Examination-Revised, which has demonstrated a valuable brief appraisal instrument for the early identification of a scope of the neurodegenerative issue including AD and FTD. It likewise has all the earmarks of being useful in foreseeing those with gentle subjective impedance who will advance to forthcoming dementia. (Hodges, 2013, p. S211)

III. Approaches to the Disorder

A. In regard to the rising pervasiveness of dementia, and the comparative deficiency of present day, accessible pharmacological treatment, the need to create and execute new treatments is squeezing. Late results from trials of specialists in AD with potential sickness altering impacts are empowering, however, should likewise be deciphered with an alert. Such pharmaceuticals could possibly defer the onset of dementia and would consequently notably decrease its pervasiveness and effect; 74 be that as it may, at present we remain a decent separation far from clinically accessible illness changing treatment. One would trust, in any case, that with progressing neuroimaging methods and biochemical biomarkers, and an improved comprehension of the hidden obsessive procedures included, this turns into a practical objective soon. Moreover, while concentrating on the advancement of new treatments is extremely welcome, we should likewise be careful that dementia is a multifaceted, complicated sickness, which by its inclination coordinates a requirement for a multidisciplinary way to deal with consideration. Our center in overseeing patients with dementia must stay balanced and comprehensive, focusing on pharmacological treatment as well as on the complex biopsychosocial parts of administering to this gathering of patients. (Briggs, Kennelly, & O’Neill, 2016, p. 251)

B. Utilizing a Systems Approach to LOAD. "We created and connected an Integrative system based way to deal with distinguishing modules of qualities connected with neurodegenerative illness. We prepared 1,647 autopsied tissues from the dorsolateral prefrontal cortex (PFC), visual cortex (VC), and cerebellum (CB) in 549 brains of 376 LOAD patients and 173 non-unhinged solid controls. All subjects were analyzed at admission, and every cerebrum experienced broad LOAD-related pathology examination. We take note of that the known APOE genotype presentation was affirmed in the Harvard Brain Tissue Resource Center (HBTRC) test, demonstrating a chances proportion of 3.74 for every duplicate ε4 allele (p = 4.1 × 10−13). Every tissue test was profiled for 39,579 transcripts speaking to 25,242 known and 14,337 anticipated quality expression attributes, and every subject genotyped for 838,958 one of a kind SNPs. Unless noted, quality expression investigations were balanced for age and sex, posthumous interim (PMI) in hours, and test pH and RNA trustworthiness number (RIN). In the general accomplice of LOAD and non-hysterical brains, the mean ± standard deviation (SD) for test PMI, pH, and RIN were 17.8 ± 8.3, 6.4 ± 0.3, and 6.8 ± 0.8, separately. A broad investigation of the impact of covariates on quality expression variety in LOAD and non-unhinged brains was completed. We utilized a vigorous, direct relapse model for covariate rectifications in all our quality expression examinations. Consequences of customary differential expression investigation exhibit that subsets of qualities were up-or downregulated in LOAD. Predictable with the known movement and local seriousness of LOAD pathology (Braak and Braak, 1991), we watched that the PFC area contained the best number of differentially communicated qualities. [Clustering analysis] abridges the bunching or collinearity of the different LOAD pathology characteristics and age inside the HBTRC companion, bringing about particular gatherings of clinical pathology and age as isolated groups. For example, the quantity of huge connections of expression characteristics to neuropathology like Braak stage inside the LOAD quiet gathering was most elevated in the PFC locale. Given these perceptions and the way that PFC is more generally influenced by LOAD than CB and VC (Braak and Braak, 1991), a specific consideration was paid to this locale in our procedure to rank-request modules for significance to LOAD. These enormous information sets were the premise of further technique advancement with the intent to recognize and rank-request system modules and quality targets connected with LOAD pathology. (Zhang, Bin et al., 2013, p. 707)

IV. Current Research

A. Possible causes

1. Age is the most grounded danger variable for cerebrum degeneration whether it results from vascular or neurodegenerative components or both. To assess the ebb and flow on the effect of vascular infection on the most well-known reasons for dementia, most pertinent articles to the chosen subject headings were investigated until November 2011 from the prominently utilized databases including Pubmed, Cochrane Database, and Biological Abstracts. Inside the previous decade, there has been four-fold expanded enthusiasm for the vascular premise of neuro-degeneration and dementia. Vascular maturing including blood vessel solidness, endothelial changes, and blood-mind boundary brokenness influences neuronal survival by impeding a few intracellular defensive instruments prompting constant hypoperfusion. Modifiable danger elements, for example, hypertension, diabetes, dyslipidemia and adiposity connected to Alzheimer's malady and vascular dementia advance the degeneration and diminish the regenerative limit of the vascular framework. These in pair with amassing of anomalous proteins, for example, amyloid β likely upset cerebral autoregulation, neurovascular coupling and perfusion of the most profound structures to variable degrees to deliver white matter changes and particular mind decay. Cerebrum neurotic changes might be further adjusted by hereditary elements, for example, the apolipoprotein E ε4 allele. The way of life measures that keep up or enhance vascular wellbeing including utilization of sound weight control plans, moderate utilization of liquor and executing standard physical activity when all is said in done seem compelling for diminishing dementia hazard. Intercessions that enhance vascular capacity are critical to support subjective status notwithstanding amid maturing while precaution measures that decrease the danger of vascular infection are anticipated to diminish the weight of dementia in the long haul. (Akinyemi, Mukaetova-Ladinska, Attems, Ihara, Kalaria, 2013, p. 642)

2. Alzheimer’s disease at the molecular level is not completely understood. There are genetic factors (genetics) that are “While molecular basis of AD is not entirely understood, genetic factors are anticipated to play a role in the developing and progression of AD. (Song, Jingwen, Sungeun, Risacher, Wong, Saykin, & Greene, 2016, pp. 1)

3. It is apparent that Aβ amassing in the CNS can be both a cause and outcome of BBB brokenness in AD. Be that as it may, other Aβ-free pathologies can phenotypically imitate BBB brokenness saw in AD and numerous adjustments in the BBB cause neurotoxicity autonomously of Aβ. This highlights the many-sided quality of AD and the probability that AD has differing etiologies that join on Aβ and tau. An absence of obvious confirmation of BBB disturbance in AD requires the thought of other basic elements of the BBB that may get to be debilitated in AD, for example, modified transport and correspondence inside the neurovascular unit. We reason that the BBB assumes a multifaceted part in AD both upstream and downstream of the amyloid course, and is along these lines essential to consider in future endeavors towards understanding this highly destructive, deadly, pandemic disease. (Erickson & Banks, 2013, p. 1513)

B. Possible treatments

1. Regardless of the outstanding general wellbeing issue that it postures, just five therapeutic medicines have been affirmed for AD, and this demonstration to control manifestations as opposed to change the course of the infection. Investigations of potential infection altering treatment have been attempted in patients with clinically distinguishable sickness, yet confirm proposes that the obsessive changes connected with AD start quite a long while before this. It is conceivable that pharmacological treatment might be beneficial in this pre-clinical stage before the neurodegenerative procedure is set up. Systems giving prior finding, for example, cerebrospinal liquid biomarkers and amyloid positron emanation tomography neuroimaging, are vital to testing this hypothesis in clinical trials. Late results from trials of specialists, for example, Aducanumab are empowering yet should likewise be deciphered with an alert. Such pharmaceuticals could defer the onset of dementia and would in this manner uniquely diminish its predominance. In any case, we as of now remain a decent separation far from clinically accessible infection altering treatment. (Briggs, Kennelly, & O’Neill, 2016, p. 247)

2. The ebb and flow discoveries show that mellow to direct Alzheimer's infection patients on a steady dosage of a cholinesterase inhibitor can profit by psychological incitement treatment. We found a noteworthy impact on insight as well as an exceedingly huge impact on two areas of neuropsychiatric unsettling influence. Examination of the ten Neuropsychiatric Inventory spaces independently demonstrated that subjective incitement treatment enhances scores on disregard and sorrow. (Niu, Tan, Guan, Zhang, & Wang, 2010, p. 1107)

3. This study is based on cognitive behavioral therapy. It utilizes a multicomponent management executed with the best in a randomly controlled research philosophy. Recently, a report regarding nationwide dementia systems reasons that any national dementia arrangement ought to incorporate, in addition to other things, the objectives of enhancing early analysis and treatment, of enhancing backing to the individual with dementia living at home, and in addition to the parental figure, and of enhancing preparing for social insurance experts [86]. This trial can set up an observationally based mental treatment for non-intellectual indications that decrease the personal satisfaction of the individual with dementia and the parental figure. The treatment manual will be distributed, and preparation workshops will be offered so that the data can be spread among human services experts. (Forstmeier, Maercker, Savaskan, & Roth, 2015.


More research is direly needed to be conducted on Alzheimer’s disease. Causes, treatments, cures, interventions, and caregiving are all areas that need immediate and ongoing studies. More and more people will be reaching 65 years and older which means that even more people will be developing Alzheimer’s if something is not done.

“The total estimated worldwide costs of dementia were US$604 billion in 2010. About 70% of the expenses occurred in western Europe and North America. In such high-income regions, costs of informal care and the direct costs of social assistance contribute similar proportions of total costs, whereas the direct medical costs were much lower. In low- and middle-income countries, informal care accounts for the majority of total expenses; direct social care costs are negligible. Worldwide costs of dementia are enormous and distributed inequitably.

There is considerable potential for cost increases in coming years as the diagnosis and treatment gap is reduced. There is also likely to be a trend in low- and middle-income countries for social care costs to shift from the informal to the formal sector, with significant implications for future aggregated costs and the financing of long-term care. Only by investing now in research and the development of cost-effective approaches to early diagnosis and care can future societal costs be anticipated and managed” (Wimo, Jonsson, Bond, Prince, & Winblad, 2013, p. 1).

Through scholarly research, this research paper has compiled valuable information about the detrimental effects that Alzheimer’s disease has on a person’s memory, historical evaluations and approaches to the disorder, possible causes and treatments, and comparisons to current research regarding possible causes and treatments.

Alzheimer’s Association. (2016). Younger/Early onset Alzheimer’s and dementia. Retrieved online at
Belsky, J. (1999). The psychology of aging (3rd ed.). Cengage. ISBN: 9780534359126.
Briggs, R., Kennelly, S. P., & O'Neill, D. (2016). Drug treatments for Alzheimer's disease. Clinical Medicine, 16(3), 247-253.
Charlesworth, L. A., Allen, R. J., Morson, S., Burn, W. K., & Souchay, C. (2014). Working memory and the enactment effect in early Alzheimer's disease. ISRN Otolaryngology, 1-5. doi:10.1155/2014/694761
Erickson, M. A. & Banks, W. A. (2013, Oct.). Blood-brain barrier dysfunction as a cause and consequence of Alzheimer’s disease. Journal of cerebral blood flow & metabolism. Vol. 33, Issue 10. doi: 10.1038/jcbfm.2013.135. Retrieved online at
Forstmeier, S., Maercker, A., Savaskan, E., & Roth, T. (2015). Cognitive behavioral treatment for mild Alzheimer's patients and their caregivers (CBTAC): study protocol for a randomized controlled trial. Trials, Vol. 16, pp. 526-539 14p. doi:10.1186/s13063-015-1043-0
Hodges, J. R. (2013). Alzheimer’s disease and the frontotemporal dementias: Contributions to clinicopathological studies, diagnosis, and cognitive neuroscience. Alzheimer’s disease: Advances for a new century. Journal of Alzheimer’s disease. Retrieved online at
Ladenson, J. H., Laterza, O., & Modur, V. (2013). Alzheimer’s diagnosis. Patents. Retrieved online at
References (cont)
Niu, Y., Tan, J., Guan, J., Zhang, Z., & Wang, L. (2010). Cognitive stimulation therapy in the treatment of neuropsychiatric symptoms in Alzheimer’s disease: A randomized controlled trial. Clinical Rehabilitation, 24(12), 1102-1111, 10p. doi:10.1177/0269215510376004
O. Akinyemi, Rufus; B. Mukaetova-Latin ska, Elizabeth; Attems, Johannes; Ihara, Masafumi; N. Kalaria, Raj. (2013, Jul.). Neurodegeneration in aging-related dementias: Alzheimer’s disease and vascular dementia. Current Alzheimer Research, Vol. 10, No. 6, pp. 642-653(12). Retrieved online at
Song, A., Jingwen, Y., Sungeun, K., Risacher, S. L., Wong, A. K., Saykin, A. J., & ... Greene, C. S. (2016). Network-based analysis of genetic variants associated with hippocampal volume in Alzheimer's disease: a study of ADNI cohorts. Biodata Mining, 91-8. doi:10.1186/s13040-016-0082-8
Wimo, Anders et al. (2013, Jan.). The worldwide economic impact of dementia 2010. Alzheimer's & Dementia: The Journal of the Alzheimer's Association. Vol. 9, Issue 1, pp. 1-11.e3. Retrieved online at
Zhang, Bin et al. (2013, Apr.). Integrated systems approach identifies genetic nodes and networks in late-onset Alzheimer’s disease. Cell. Vol. 153, Issue 3, pp. 707 – 720.
Retrieved online at


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