title: Does accumulation of advanced glycation end products contribute to the aging phenotype?
abstract: BACKGROUND
  Aging is a complex multifactorial process characterized by accumulation of deleterious changes in cells and tissues, progressive deterioration of structural integrity and physiological function across multiple organ systems, and increased risk of death.
  
  
  METHODS
  We conducted a review of the scientific literature on the relationship of advanced glycation end products (AGEs) with aging. AGEs are a heterogeneous group of bioactive molecules that are formed by the nonenzymatic glycation of proteins, lipids, and nucleic acids.
  
  
  RESULTS
  Humans are exposed to AGEs produced in the body, especially in individuals with abnormal glucose metabolism, and AGEs ingested in foods. AGEs cause widespread damage to tissues through upregulation of inflammation and cross-linking of collagen and other proteins. AGEs have been shown to adversely affect virtually all cells, tissues, and organ systems. Recent epidemiological studies demonstrate that elevated circulating AGEs are associated with increased risk of developing many chronic diseases that disproportionally affect older individuals.
  
  
  CONCLUSIONS
  Based on these data, we propose that accumulation of AGEs accelerate the multisystem functional decline that occurs with aging, and therefore contribute to the aging phenotype. Exposure to AGEs can be reduced by restriction of dietary intake of AGEs and drug treatment with AGE inhibitors and AGE breakers. Modification of intake and circulating levels of AGEs may be a possible strategy to promote health in old age, especially because most Western foods are processed at high temperature and are rich in AGEs.
authors.affiliation: Department of Ophthalmology, Johns Hopkins University School of Medicine, Smith Building, M015, 400 North Broadway, Baltimore, MD 21287, USA. rdsemba@jhmi.edu
authors.forename: Richard D
authors.initials: RD
authors.lastname: Semba
authors.forename: Emily J
authors.initials: EJ
authors.lastname: Nicklett
authors.forename: Luigi
authors.initials: L
authors.lastname: Ferrucci
mesh_terms: D000375:Aging / Q000378:metabolism*; D001842:Bone and Bones / Q000378:metabolism; D001921:Brain / Q000378:metabolism; D004032:Diet; D004791:Enzyme Inhibitors / Q000494:pharmacology; D004912:Erythrocytes / Q000378:metabolism; D005123:Eye / Q000378:metabolism; D005504:Food Analysis; D017127:Glycation End Products, Advanced / Q000037:antagonists & inhibitors / Q000378:metabolism*; D006146:Guanidines / Q000494:pharmacology; D006801:Humans; D007249:Inflammation / Q000378:metabolism; D007668:Kidney / Q000378:metabolism; D008099:Liver / Q000378:metabolism; D008136:Longevity; D018482:Muscle, Skeletal / Q000378:metabolism; D009206:Myocardium / Q000378:metabolism; D018384:Oxidative Stress / Q000502:physiology; D000067759:Receptor for Advanced Glycation End Products; D011971:Receptors, Immunologic / Q000378:metabolism; D013710:Tendons / Q000378:metabolism; D013844:Thiazoles / Q000494:pharmacology
chemical_list: D004791:Enzyme Inhibitors; D017127:Glycation End Products, Advanced; D006146:Guanidines; D000067759:Receptor for Advanced Glycation End Products; D011971:Receptors, Immunologic; D013844:Thiazoles; C406794:alagebrium; C004479:pimagedine