scholarly journals The promise of microRNA-based therapies in Alzheimer’s disease: challenges and perspectives

2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Hannah Walgrave ◽  
Lujia Zhou ◽  
Bart De Strooper ◽  
Evgenia Salta
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Clinical Applications ◽  
Toxic Effects ◽  
Microrna Regulation ◽  
Research Findings ◽  
Fundamental Research ◽  
Initial Discovery ◽  
Regulatory Potential

AbstractMulti-pathway approaches for the treatment of complex polygenic disorders are emerging as alternatives to classical monotarget therapies and microRNAs are of particular interest in that regard. MicroRNA research has come a long way from their initial discovery to the cumulative appreciation of their regulatory potential in healthy and diseased brain. However, systematic interrogation of putative therapeutic or toxic effects of microRNAs in (models of) Alzheimer’s disease is currently missing and fundamental research findings are yet to be translated into clinical applications. Here, we review the literature to summarize the knowledge on microRNA regulation in Alzheimer’s pathophysiology and to critically discuss whether and to what extent these increasing insights can be exploited for the development of microRNA-based therapeutics in the clinic.

The Dissemination of Research Findings: Some Limitations Revealed When Attempting a Meta-Analysis

1986 ◽  
Vol 20 (3) ◽  
pp. 384-385 ◽  
Author(s):  
A. F. Jorm
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Meta Analysis ◽  
Descriptive Statistics ◽  
Additional Information ◽  
Dissemination Of Research ◽  
Drug Treatments ◽  
Research Findings

A meta-analysis of the literature on drug treatments for Alzheimer's disease revealed the following limitations in the dissemination of research findings: multiple publication of findings, failure to report basic descriptive statistics and failure to respond to written requests for additional information on the research. The possible reasons for these problems and remedies for them are discussed.

scholarly journals Towards the prevention of potential aluminum toxic effects and an effective treatment for Alzheimer's disease

2011 ◽  
Vol 105 (11) ◽  
pp. 1505-1512 ◽  
Author(s):  
Maire E. Percy ◽  
Theo P.A. Kruck ◽  
Aileen I. Pogue ◽  
Walter J. Lukiw
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Effective Treatment ◽  
Toxic Effects

scholarly journals Seeking a New Paradigm for Alzheimer’s Disease: Considering the Roles of Inflammation, Blood-Brain Barrier Dysfunction, and Prion Disease

2017 ◽  
Vol 2017 ◽  
pp. 1-6
Author(s):  
Mark E. McCaulley ◽  
Kira A. Grush
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Prion Disease ◽  
Effective Means ◽  
Neurovascular Unit ◽  
New Paradigm ◽  
Barrier Dysfunction ◽  
Effective Prophylaxis ◽  
Research Findings ◽  
Current Paradigm

There is no effective etiologic treatment for Alzheimer’s disease, nor is there a prophylactic medication which delays or prevents its onset. The lack of an accurate paradigm is undoubtedly related to the lack of effective means of prophylaxis and treatment. The current paradigm of beta amyloid in Alzheimer’s brains causing cognitive dysfunction must be modified. Despite failed clinical trials, research continues into amyloid-oriented treatments. The persistence of the amyloid hypothesis/paradigm is an example of anchoring and representativeness heuristics described by Kahneman and Tversky in their classic 1974 Science paper. Economic factors also contribute to the persistence of this paradigm. Paradigms impact the scientific process by the following: (1) what is studied; (2) the types of questions that are asked; (3) the structure and nature of the questions; (4) the interpretations of research findings. We review the contribution of inflammation, malfunction of the neurovascular unit, and prion disease to Alzheimer’s disease manifestations. Any or all of these are candidates for inclusion into a more accurate, inclusive, and useful new paradigm. By incorporating emerging facts and understanding into a new paradigm, we will enhance our ability to move toward effective prophylaxis and therapy for this tragic disease.

Research Findings

2005 ◽  
Vol 09 (09) ◽  
pp. 368-372
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cervical Cancer ◽  
Gene Therapy ◽  
Nk Cells ◽  
Human Genome ◽  
New Method ◽  
Elephant Shark ◽  
Research Findings ◽  
Insight Into

Forthcoming: A Vaccine for Cervical Cancer. A Safer and More Effective "Aspirin". Scientists Uncover A New Method of Producing NK Cells. Insight into the Human Genome Through the Elephant Shark. Using Gene Therapy for Alzheimer's Disease.

scholarly journals In Vivo Imaging Biomarkers in Mouse Models of Alzheimer's Disease: Are We Lost in Translation or Breaking Through?

2010 ◽  
Vol 2010 ◽  
pp. 1-11 ◽  
Author(s):  
Benoît Delatour ◽  
Stéphane Epelbaum ◽  
Alexandra Petiet ◽  
Marc Dhenain
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Models ◽  
Imaging Biomarkers ◽  
Preclinical Research ◽  
Disease Modifier ◽  
Fundamental Research ◽  
Neuroimaging Biomarkers ◽  
Lost In Translation

Identification of biomarkers of Alzheimer's Disease (AD) is a critical priority to efficiently diagnose the patients, to stage the progression of neurodegeneration in living subjects, and to assess the effects of disease-modifier treatments. This paper addresses the development and usefulness of preclinical neuroimaging biomarkers of AD. It is today possible to image in vivo the brain of small rodents at high resolution and to detect the occurrence of macroscopic/microscopic lesions in these species, as well as of functional alterations reminiscent of AD pathology. We will outline three different types of imaging biomarkers that can be used in AD mouse models: biomarkers with clear translational potential, biomarkers that can serve as in vivo readouts (in particular in the context of drug discovery) exclusively for preclinical research, and finally biomarkers that constitute new tools for fundamental research on AD physiopathogeny.

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