Psychology: Amyloid Deposition and Alzheimer’s Disease
This critique examines the research study reported by Hardy and Selkoe (2002). The study explored the relationship between Amyloid concentrations and Alzheimer’s disease (AD) among clinical patients. The purpose of this critique is to re-examine the viability of the hypothesis that links Amyloid with Alzheimer’s disease.
The paper examines the weaknesses and strengths of the hypothesis with the aim of establishing whether the given conclusions on the study are real and applicable. This critique intends to establish the viability of the research article by analyzing the strengths and weaknesses of the entire research paper.
The title of the report The Amyloid Hypothesis of Alzheimer’s Disease: Progress and Problems on the Road to Therapeutics adequately explores the Amyloid hypothesis as the key subject of interest. Major variables to be addressed in the paper are also clear in the title of the research study. They include the progress and problems associated with Alzheimer’s disease in relation to the hypothesis (Kastin, 2013).
The main features of the study are not offered clearly in the abstract. The abstract lacks information on how the study was conducted, as well as the various methods that were used. However, the abstract presents the link between Amyloid and the development of Alzheimer’s disease. It also identifies the factors that contribute towards its progression. It is, therefore, a viable abstract for the study.
Hypothesis and results
The researchers clearly presented the hypothesis of the study. Hardy and Selkoe (2002) observe that “now that therapies based on this idea are beginning to enter human trials, it is important that we critically re-examine the Amyloid hypothesis and address its strengths and weaknesses, both real and perceived.” The latter statement sufficiently supported the need for conducting a study of this nature.
The significance of the study for medical application is based on the argument that the hypothesis is already undergoing clinical trials and that the analysis of the hypothesis will enable the medical practitioners to make informed decision on whether to fully adopt the hypothesis or carry out further research in order to ascertain the viability of the hypothesis (Linda, Juergen & Bludau, 2011).
The researchers concluded that the viability of the Amyloid hypothesis in relation to the development of AD has some shortfalls. However, the study admits that there is no better alternative to causative agents of AD.
The argument is that the available theories are not well researched and therefore pose a lot of doubt on the validity of the alternatives (Kastin, 2013). The authors arrived at this conclusion after examining various strengths and weaknesses of the hypothesis.
Several pieces of evidence that link AD to Amyloid have been presented in the study. For instance, minimal effects that occur due to severe changes in the tau protein limit its link to AD.
Secondly, the change in APP synthesis takes place before changes in the tau protein among AD patients. Thirdly, there is a close link between the genetic effects of AD infection with the metabolism of Amyloid. In addition, the late onset of AD is associated with the catabolism of Amyloid (Harris & Fahrenholz, 2005).
The researchers raise concerns on the assumptions that Amyloid synthesis and metabolism are responsible for the development of AD. The authors argue that the concentrations of Amyloid in the brain are not directly proportional to the level of brain degradation due to the presence of AD. Moreover, the concentration of Amyloid is increased by all mutations that cause AD.
However, there is no connection between the mutations and the age at which the affected individuals start experiencing the problem (Harris & Fahrenholz, 2005). Moreover, other diseases emerge due to increased metabolism of the Amyloid protein that usually worsens the effects of the Amyloid synthesis in the body.
Furthermore, the age at which the symptoms of AD occur has been attributed to genetic factors and not the concentrations of Amyloid. In addition, the authors note that there is a lack of information on the available species of Amyloid that are associated with the development of AD. They further ascertain that there is no actual information on how the concentration of this protein affects the brain system.
These facts are used by the authors in developing the hypothesis and conclusion of the study. The conclusion has been arrived at by analyzing the various source of information on Amyloid. Other factors that may contribute to the development of AD are also described in the research study.
Research Methods and approaches
The research method used in this study is non-experimental in nature (Harris & Fahrenholz, 2005). The researchers employ critical analysis of the evidence tabled on the theory about AD through a detailed literature review. This approach is appropriate in ascertaining the loopholes in the theory.
In terms of probing the literature review, it was noted that the majority of the sources used were primary in nature. The authors analyzed several research journal articles in order to obtain the basis of their hypothesis. This information enabled the authors to establish a credible presentation of information sourced from various research studies.
In addition, the bulk of references incorporated in the study and referred to in the evaluation of the literature were published from 1990 to 2002. The latter represented a synthesis of the existing evidence on the subject of the relationship between Amyloid concentrations and Alzheimer’s disease among clinical patients.
The information presented in the literature review is substantial in creating doubt on the theory linking Amyloid to AD. It also offers a leeway for further research to be conducted, and the gaps presented by the review dealt with before the full implementation of clinical approaches of AD theory. The research is, therefore, applicable in the analysis of the effects of Amyloid in relation to AD (Harris & Fahrenholz, 2005).
The approach adopted in this study involves the analysis of various credible research articles. These articles are based on researches conducted on AD and Amyloid. All the relevant facts on AD have been presented by various research studies. The articles used in the research study offer a detailed review of the development and effects of Amyloid.
Consequently, the authors are capable of drawing a concise conclusion based on the facts presented in the articles. The study revealed various possibilities of causative factors of AD and compared these factors to Amyloid. Lack of adequate information on the other cause and hypothesis of AD left the authors with minimal options to explore.
Recommendations and conclusion
The study was relevant since it managed to present the strengths and weaknesses of the Amyloid Hypothesis. The study also ascertained the limitations of the theory (Kastin, 2013). The manner in which the authors presented information on the various stages of AD and the available system changes that may instigate the condition are clear indications that the paper was fully researched.
Information on the early stages of the disease, genetic factors that increase the probability of being infected by the disease, and the dissociation of the stage of development of the disease from Amyloid prevalence were properly documented in the paper. The authors also offered a detailed analysis of Amyloid.
The information presented in the article is adequate to deduce the relationship between AD and the proteins. These facts resulted in the conclusion that the link between AD and Amyloid is still uncertain.
I ended up agreeing with the author that before the anti-amyloid therapy is adopted fully as a clinical procedure of handling Alzheimer’s disease, other alternatives have to be analyzed. Furthermore, the weaknesses of the theory presented by the study need to be addressed before fully implementing the procedure.
However, the study could have been improved by conducting an experimental analysis of the problem statement. The use of a real sample population that involves patients, their siblings, and adults who are not infected may enhance the findings of the study (Harris & Fahrenholz, 2005).
Information on hereditary factors associated with the disease could have been analyzed in this case. The use of family history and other predisposing factors in the sample population analysis could have enriched the study. It is obvious that if the authors could have adopted this approach, a different conclusion may have been reached.
They could have offered a better recommendation rather than simply justifying that the Amyloid hypothesis is still the best alternative in spite of the fact that other theories have not been studied accordingly.
In conclusion, it is vital to reiterate that the study is informative. I believe that it offers the necessary guidelines needed in dealing with a disorder that has affected humanity for several decades (Linda, Juergen & Bludau, 2011).
Hardy, J. & Selkoe, D. J. (2002). The Amyloid Hypothesis of Alzheimer’s Disease: Progress and Problems on the Road to Therapeutics. Science, 297, 353-356
Harris, J. R. & Fahrenholz, F. (2005). Alzheimer’s Disease: Cellular and Molecular Aspects of Amyloid. New York, NY: Springer
Kastin, A. (2013). Handbook of Biologically Active Peptides. Waltham, Massachusetts: Academic Press
Linda, C., Juergen H., & Bludau M. D. (2011). Alzheimer’s Disease: Biographies of disease. Santa Barbara, California: ABC-CLIO.
Leave a ReplyWant to join the discussion?
Feel free to contribute!