ISSN: 2168-9296
Cell & Developmental Biology
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Cellular Pathology of Alzheimer Disease

Elizabeth A. Perry and George Perry*
Semmes Foundation, Distinguished Chair in Neurobiology College of Sciences, The University of Texas at San Antonio, USA
Corresponding Author : George Perry
Dean and Professor, Semmes Foundation
Distinguished Chair in Neurobiology College of Sciences The University of Texas at San Antonio, USA
Tel: 210-458-4450
Fax: 210-458-4445
E-mail: george.perry@utsa.edu
Received: August 11, 2015; Accepted: August 12, 2015; Published: August 19, 2015
Citation: Perry E A, Perry G (2015) Cellular Pathology of Alzheimer Disease. Cell Dev Biol 4:e134. doi:10.4172/2168-9296.1000e134
Copyright: © 2015 Perry G etal. 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.
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Editorial
The pathology of Alzheimer’s disease largely remains a mystery awaiting new methods to make breakthrough discoveries. Where so much of today’s work focuses on the brain as a whole, much of disease takes place on a cellular level. Seemingly innocent molecular changes alter the biochemistry and metabolism of individual pathways. Steps involving amplification can perpetuate these abnormalities to signal catastrophe to the individual cell. As individual cells shift away from homeostasis, the entire tissue or organ may change in its functional capacity.
So what are these small cellular changes, and are they always the culprit in disease? Not necessarily. The cell is a highly dynamic microenvironment, filled with many organelles that serve to further compartmentalize the biological reactions of life. Often times, metabolic shifts may serve as a method of cellular protection and a way to survive in the face of stress. In order to understand the pathophysiology of AD, we need to examine changes on the cellular level and ask ourselves what may serve as a stimulus for these changes. Are these changes really the cause of the disease? Or are they the cell’s compensation against a much more powerful force?
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