Ilya Bezprozvanny & Mark P. Mattson on the Importance of Calcium
Fast Moving Front Commentary, September 2010
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Article: Neuronal calcium mishandling and the pathogenesis of Alzheimer's disease
Authors: Bezprozvanny, I;Mattson, MP |
Ilya Bezprozvanny & Mark P. Mattson talk with ScienceWatch.com and answer a few questions about this month's Fast Moving Fronts paper in the field of Neuroscience & Behavior.
Why do you think your paper is highly
cited?
There are two main reasons our paper is highly cited. First, calcium plays major roles in the formation and function of neuronal circuits, including those involved in learning and memory. Second, recent findings suggest that abnormal calcium signaling plays an important role in Alzheimer's disease (AD) pathogenesis. Our review summarized our current understanding of how abnormalities in the ability of neurons to regulate calcium signaling contribute to cognitive impairment in AD.
Does it describe a new discovery, methodology, or synthesis of knowledge?
Coauthor Mark P.
Mattson.
Read a Fast Breaking Paper
commentary (Aug. 2005), and a Classic Science
Watch Newsletter
interview with Mark P. Mattson.
This is a review that described synthesis of knowledge. Our main effort was to summarize and critically analyze the latest findings related to the "calcium hypothesis of AD" and to provide insight into the implications of this hypothesis for the development of new approaches for the prevention and treatment of AD.
Would you summarize the significance of your paper in layman's terms?
By synthesizing research findings in the areas of calcium signaling and AD, this article provides a foundation for future research aimed at developing novel therapeutic interventions for AD.
How did you become involved in this research, and how would you describe the particular challenges, setbacks, and successes that you've encountered along the way?
Both of our laboratories are actively involved in research on calcium signaling and AD. AD is a complex disorder that can result from multiple factors—genetic and environmental. It is possible to model some aspects of the disease in mice, but it is very difficult to have a complete model of AD. As a result, most studies of AD pathogenesis only provide partial information about underlying causes of the disease.
Where do you see your research leading in the future?
We will continue to advance "calcium hypothesis of AD" and we hope that in the future our experiments will help to identify therapeutic targets for AD treatment.
Do you foresee any social or political implications for your research?
Yes. The costs of care for AD patients are very large and continue to
increase every year with the aging population. This is the largest unmet
medical need in US and in other developed countries. Without complete
understanding of AD pathogenesis, effective therapies cannot be developed.
We hope that our research on calcium and AD can help to solve this enormous
social and financial problem.
Ilya Bezprozvanny, Ph.D., D.Sci.
Professor of Physiology
Carla Cocke Francis Professor in Alzheimer's
Research
Department of Physiology
UT Southwestern Medical Center at Dallas
Dallas, TX, USA
Mark P. Mattson, Ph.D.
Chief, Laboratory of Neurosciences, National Institute on
Aging
Laboratory of Neurosciences - NIA
Biomedical Research Center
Baltimore, MD, USA
ADDITIONAL INFORMATION:
- Read a Fast Breaking Paper commentary (Aug. 2005), and a Classic Science Watch Newsletter interview (Sep. 2003) with Mark P. Mattson.
KEYWORDS: NEURONAL CALCIUM, PATHOGENESIS, ALZHEIMER'S DISEASE, AMYLOID BETA PEPTIDE, CULTURED HIPPOCAMPAL NEURONS, PRECURSOR PROTEIN, TRANSGENIC MICE, MOUSE MODEL, MITOCHONDRIAL DYSFUNCTION, NICOTINIC RECEPTORS, RYANODINE RECEPTOR.