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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.

journal of cerebral blood flow and metabolism

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