Advanced Glycation Endproducts Induce Changes in Glucose Consumption, Lactate Production, and ATP Levels in SH-SY5Y Neuroblastoma Cells by a Redox-Sensitive Mechanism

Advanced glycation endproducts (AGEs) accumulate on long-lived proteins, including β-amyloid plaques in Alzheimer's disease, and are suggested to contribute to neuronal dysfunction and cell death. We have investigated the effects of a model AGE upon glucose metabolism and energy production in a neuroblastoma cell line. AGEs decrease cellular ATP levels and increase glucose consumption and lactate production. All of the AGE-induced metabolic changes can be attenuated by antioxidants such as (R+)-α-lipoic acid and 17β-estradiol. These antioxidants may become useful drugs against (AGE-mediated) effects in neurodegeneration through their positive effects on cellular energy metabolism.