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| Title: | Oxidative stress in diabetes and alzheimer’s disease |
| Author (s): | Reddy, Prakash Zhu, Xiongwei Perry, George Smith, Mark A. |
| Department/Lab Affiliations: | Center for Environmental Science and Technology (CEST) Chemistry |
| Keywords: | AGE inhibitors advanced glycation end products glycation protein crosslinks |
| Subject Terms: | Alzheimer's disease. Diabetes. Glycosylation. Maillard reaction. Oxidative stress. |
| Issue Date: | 2009 |
| Publisher: | IOS Press |
| Citation: | Reddy, V. Prakash, Xiongwei Zhu, George Perry, and Mark A. Smith. “Oxidative Stress in Diabetes and Alzheimer’s Disease”, Journal of Alzheimer's Disease, Vol. 16, No. 4, (2009): 763-774. |
| Abstract: | Oxidative stress plays a major role in diabetes as well as in Alzheimer's disease and other related neurological diseases. Intracellular oxidative stress arises due to the imbalance in the production of reactive oxygen/reactive nitrogen species and cellular antioxidant defense mechanisms. In turn, the excess reactive oxygen/reactive nitrogen species mediate the damage of proteins and nucleic acids, which have been shown to have direct and deleterious consequences in diabetes and Alzheimer's disease. Oxidative stress also contributes to the production of advanced glycation end products through glycoxidation and lipid peroxidation. The advanced glycation end products and lipid peroxidation products are ubiquitous to diabetes and Alzheimer's disease and serve as markers of disease progression in both disorders. Antioxidants and advanced glycation end products inhibitors, either induced endogenously or exogenously introduced, may counteract with the deleterious effects of the reactive oxygen/reactive nitrogen species and thereby, in prevention or treatment paradigms, attenuate or substantially delay the onset of these devastating pathologies. |
| Type: | Article - Journal text |
| In Title: | Journal of Alzheimer's Disease |
| Copyright Notice: | This material is presented to ensure timely dissemination of scholarly and technical work. Copyright and all rights therein are retained by authors or by other copyright holders. All persons copying this information are expected to adhere to the terms and constraints invoked by each author's copyright. In most cases, these works may not be reposted without the explicit permission of the copyright holder. Pre-print: author can archive; Post-print: author can archive; FULL COPYRIGHT INFORMATION: |
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| title | Oxidative stress in diabetes and alzheimer’s disease |
| contributor.author | Reddy, Prakash |
| contributor.author | Zhu, Xiongwei |
| contributor.author | Perry, George |
| contributor.author | Smith, Mark A. |
| contributor.deptlab | Center for Environmental Science and Technology (CEST) |
| contributor.deptlab | Chemistry |
| subject | AGE inhibitors |
| subject | advanced glycation end products |
| subject | glycation |
| subject | protein crosslinks |
| subject.LCSH | Alzheimer's disease. |
| subject.LCSH | Diabetes. |
| subject.LCSH | Glycosylation. |
| subject.LCSH | Maillard reaction. |
| subject.LCSH | Oxidative stress. |
| date.issued | 2009 |
| publisher | IOS Press |
| identifier.citation | Reddy, V. Prakash, Xiongwei Zhu, George Perry, and Mark A. Smith. “Oxidative Stress in Diabetes and Alzheimer’s Disease”, Journal of Alzheimer's Disease, Vol. 16, No. 4, (2009): 763-774. |
| identifier.pub.URI | |
| description.abstract | Oxidative stress plays a major role in diabetes as well as in Alzheimer's disease and other related neurological diseases. Intracellular oxidative stress arises due to the imbalance in the production of reactive oxygen/reactive nitrogen species and cellular antioxidant defense mechanisms. In turn, the excess reactive oxygen/reactive nitrogen species mediate the damage of proteins and nucleic acids, which have been shown to have direct and deleterious consequences in diabetes and Alzheimer's disease. Oxidative stress also contributes to the production of advanced glycation end products through glycoxidation and lipid peroxidation. The advanced glycation end products and lipid peroxidation products are ubiquitous to diabetes and Alzheimer's disease and serve as markers of disease progression in both disorders. Antioxidants and advanced glycation end products inhibitors, either induced endogenously or exogenously introduced, may counteract with the deleterious effects of the reactive oxygen/reactive nitrogen species and thereby, in prevention or treatment paradigms, attenuate or substantially delay the onset of these devastating pathologies. |
| type | Article - Journal |
| type.DCMIType | text |
| type.status | Postprint |
| relation.isPartOf | Journal of Alzheimer's Disease |
| rights | This material is presented to ensure timely dissemination of scholarly and technical work. Copyright and all rights therein are retained by authors or by other copyright holders. All persons copying this information are expected to adhere to the terms and constraints invoked by each author's copyright. In most cases, these works may not be reposted without the explicit permission of the copyright holder. |
| rights | Pre-print: author can archive; Post-print: author can archive; |
| rights.URI | |
| identifier.persist.URI | |
| date.available | 2009-09-18T19:14:14Z |