Controversy in its Essence: The Alzheimer's Paradigm in Clinical Diagnosis and Research

Bajic P Vladan^*

Institute for Pharmaceutical Research and Development, University of Belgrade and Galenika a.d, Serbia

Corresponding Author:

Bajic P Vladan
Institute for Pharmaceutical Research and Development
University of Belgrade and Galenika a.d, Serbia
Tel: 381(11) 2459 503
Fax: 381(11) 2459 503
E-mail: vladanbajic@yahoo.com

Received date: September 11, 2013; Accepted date: September 13, 2013; Published date: September 18, 2013

Citation: Vladan BJ (2013) Controversy in its Essence: The Alzheimer’s Paradigm in Clinical Diagnosis and Research. J Clin Diagn Res 1:e102. doi:10.4172/jcdr.1000e102

Copyright: © 2013 Vladan BJ. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Visit for more related articles at JBR Journal of Clinical Diagnosis and Research

Journal of Clinical Diagnosis and Research is an international journal to be launched this year and is dedicated to promote basic research in the effectiveness of medications, devises, diagnostic products and clinical research and treatment for prevention, diagnosis and relieving symptoms of disease.

When we look into the world today, we can see a trend of clinical diseases accompanied by aging in a population that is still growing. I wish here to give a glimpse of a new Journal, Journal of Clinical Diagnosis and Research and how it may affect the diagnosis and clinical treatment of Alzheimer’s disease, a disease that I’m investigating the last 12 years.

Pursuing the goal to reach a threshold in the science of Alzheimer’s disease is a front that is on going for more than a century when German psychiatrist and neuropathologist Alois Alzheimer in 1906 first described two pathological properties, the amyloid and Tau fibrils in the affected brain of the first patient Auguste Deter [1]. Two forms of AD are in the arena of research, one is the genetically bound form that relates to changes on chromosome 21, 14 and 1 affecting the APP and/or Presenilin genes, and this form is known as the familiar form of AD, or FAD. The other, more prevalent form or sporadic AD (SAD) is prevalent in people over 65 years of age. In 2006, there were 26.6 million sufferers worldwide. Alzheimer’s is predicted to affect 1 in 85 people globally by 2050 [2-4]. AD is becoming an important social problem with direct and indirect costs estimating that the costs of care for Alzheimer patients in the United States alone may be $100 billion each year [3,4]. So, the foundation of understanding AD is laid on journals expressing research, on the pharmaceutical industry and the caregivers. When we look at the trend of research papers versus the curve of AD growth in the world population, we may conclude that even though a number of research papers has grown rapidly in last two decades from 3000 publications in 1992 to more than 5000 publication in 2013, the number of journals that focus on AD and other dementia in respect to their clinical and diagnostic news is limited.

So, in order to meet the fast growing and advanced technologies in pathogenesis, diagnosis and prognosis of AD and other dementias, a comprehensive and periodical platform as the Journal of Clinical Diagnosis and Research will satisfy the need to provide unique and updated in-formation in this field. Journal of Clinical Diagnosis and Research is a new quarterly scientific journal to share and discuss new issues, findings and advanced developments in Clinical Diagnosis and Research in Diseases affecting the human population.

We wish to give the Journal a strong and novel property in the field of clinical treatment and diagnosis. In absolute scientific and pragmatic manner we wish to promote diverse views on disease treatment. As such I wish to use the Alzheimer Disease paradigm controversy, i.e. the controversy lies in the question: “Is the amyloid beta a sole intrinsic factor leading to AD as most researchers suggest or is it coupled with other factors?”

A number of researchers [5] have proposed alternative hypothesis to the AD paradigm. One is that the amyloid has a protective role in oxidative stress which is the trigger for neuronal toxicity [6]. In this essence, other proteins have been and are explored as suitable biomarkers for early AD screening schemes [7,8].

The Journal of Clinical Diagnosis and Research has a mission and a vision to pursue new views on the controversy of the Abeta hypothesis in AD and related dementia [8] by addressing novel techniques of brain imaging now available through structural MRI, molecular neuroimaging with PET, and cerebrospinal fluid analyses for clinical diagnosis and elevating research for new biomarkers giving the opportunity to other strategies for AD treatment. The Journal will highlight research and new criteria to the many drugs in development that are directed at changing pathogenesis, particularly at the production and clearance of amyloid β as well as at the hyperphosphorylation state of tau. Validation studies in existing and prospective cohorts are needed to advance these criteria and optimize their sensitivity, specificity, and accuracy.

The Journal of Clinical Diagnosis and Research is determined by its highly recognized editorial board and vision to be on the frontline of the AD controversy providing initiatives in peer reviewed research articles to address a number cumber stones in AD research such as patient-oriented research, translational presence and bring a awareness to the social problem that AD brings to all societies in the world.

The future holds a promise to our readers to broaden our global representation, maintain the quality of our articles, and those who by submitting their manuscripts are supporting our efforts to make this a premier and respected journal.

We thank both the reviewers, without whom we would not be able to address a highly representation of results in various fields of research.

References

1. Berchtold NC, Cotman CW (1998) Evolution in the Conceptualization of Dementia and Alzheimer's Disease: Greco-Roman Period to the 1960s. Neurobiol Aging 19: 173–189.
2. Brookmeyer R, Gray S, Kawas C ( 1998) Projections of Alzheimer's Disease in the United States and the Public Health Impact of Delaying Disease Onset. American Journal of Public Health 88: 1337–1342.
3. Brookmeyer R, Johnson E, Ziegler-Graham K, MH Arrighi (2007) Forecasting the global burden of Alzheimer's disease. Alzheimer's and Dementia 3: 186–191.
4. Meek PD, McKeithan K, Schumock GT (1998) Economic Considerations in Alzheimer's Disease. Pharmacotherapy 18: 68–73.
5. Castellani RJ, Petersen RB, Lee HG, Zhu X (2011) . Smith: the scientist, the man. Int J Exp Pathol. 92: 297-298.
6. Castellani RJ, Lee HG, Siedlak SL, Nunomura A et al. (2009) Reexamining Alzheimer's disease: evidence for a protective role for amyloid-beta protein precursor and amyloid-beta. J Alzheimers Dis 18: 447-452.
7. Perrin RJ, Payton JE, Malone JP, Gilmore P, Alan davis et al. (2013) Quantitative Label-Free Proteomics for Discovery of Biomarkers in Cerebrospinal Fluid: Assessment of Technical and Inter-Individual Variation. 8: 64314
8. Marialessandra Contino, Mariangela Cantore, Marcello Leopoldo Nicola Antonio Colabufo (2013) Biomarkers for the early diagnosis of Alzheimer’s disease: The challenge of XXI century. Advances in Alzheimer’s Disease 2: 13-30.