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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Swamy, Shobha Uribarri, Jaime Woodward, Mark Cai, Weijing Kuchel, George A. Chen, Xue Schnaider-beeri, Michal Simonaro, Calogera Zhu, Li Vlassara, Helen Grosjean, Fabrizio Zhao, Zhengshan Striker, Gary E. |
| Description | Author Affiliation: Cai W ( Department of Geriatrics, Division of Experimental Diabetes, Medicine, Human Genetics, and Psychiatry, The Icahn School of Medicine at Mount Sinai, New York, NY 10029.); |
| Abstract | Age-associated dementia and Alzheimer's disease (AD) are currently epidemic. Neither their cause nor connection to the metabolic syndrome (MS) is clear. Suppression of deacetylase survival factor sirtuin 1 (SIRT1), a key host defense, is a central feature of AD. Age-related MS and diabetes are also causally associated with suppressed SIRT1 partly due to oxidant glycotoxins [advanced glycation end products (AGEs)]. Changes in the modern diet include excessive nutrient-bound AGEs, such as neurotoxic methyl-glyoxal derivatives (MG). To determine whether dietary AGEs promote AD, we evaluated WT mice pair-fed three diets throughout life: low-AGE (MG(-)), MG-supplemented low-AGE (MG(+)), and regular (Reg) chow. Older MG(+)-fed mice, similar to old Reg controls, developed MS, increased brain amyloid-ß42, deposits of AGEs, gliosis, and cognitive deficits, accompanied by suppressed SIRT1, nicotinamide phosphoribosyltransferase, AGE receptor 1, and PPARγ. These changes were not due to aging or caloric intake, as neither these changes nor the MS were present in age-matched, pair-fed MG(-) mice. The mouse data were enhanced by significant temporal correlations between high circulating AGEs and impaired cognition, as well as insulin sensitivity in older humans, in whom dietary and serum MG levels strongly and inversely associated with SIRT1 gene expression. The data identify a specific AGE (MG) as a modifiable risk factor for AD and MS, possibly acting via suppressed SIRT1 and other host defenses, to promote chronic oxidant stress and inflammation. Because SIRT1 deficiency in humans is both preventable and reversible by AGE reduction, a therapeutic strategy that includes AGE reduction may offer a new strategy to combat the epidemics of AD and MS. |
| ISSN | 00278424 |
| e-ISSN | 10916490 |
| Journal | Proceedings of the National Academy of Sciences of the United States of America |
| Issue Number | 13 |
| Volume Number | 111 |
| Language | English |
| Publisher | National Academy of Sciences |
| Publisher Date | 2014-04-01 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Dementia Pathology Glycosylation End Products, Advanced Adverse Effects Metabolic Syndrome X Pyruvaldehyde ADAM Proteins Genetics Metabolism Administration, Oral Advanced Glycosylation End Product-Specific Receptor Amyloid Precursor Protein Secretases Amyloid Beta-Peptides Animals Brain Drug Effects Physiopathology Cognition Cytokines Blood Gliosis Administration & Dosage Toxicity Insulin Pharmacology Membrane Proteins Memory Mice Mice, Inbred C57BL Nicotinamide Phosphoribosyltransferase Oxidative Stress PPAR Gamma Receptors, Immunologic Sirtuin 1 Antagonists & Inhibitors Time Factors Transcription, Genetic Research Support, N.I.H., Extramural Multidisciplinary |
| Content Type | Text |
| Resource Type | Article |
| Subject | Multidisciplinary |
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