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Cellular effects of advanced glycation endproducts in Alzheimers disease--energy depletion and inflammation


, : Cellular effects of advanced glycation endproducts in Alzheimers disease--energy depletion and inflammation. Society for Neuroscience Abstracts 26(1-2): Abstract No -763 16

Advanced glycation endproducts (AGEs) accumulate on long-lived protein deposits such as beta-amyloid plaques in Alzheimer's disease brain. It is now likely, that AGEs contribute to the neuronal dysfunction and cell death in Alzheimer's disease. We show that AGEs cause: a, a dose-dependent inhibition of mitochondrial respiration (starting at 50 muM AGE), resulting in depletion of ATP and reduced glutathione as demonstrated in SHSY 5Y neuroblastoma cells, b, a dose-dependent activation of microglia (starting at 1 muM AGE) with the resulting up-regulation of the expression of neurotoxic cytokines and increased free radical production, particularly nitric oxide, as demonstrated in N-11 mouse microglia cells. Membrane permeable antioxidants such as thioctic acid, Gingko biloba extract and 17beta-estradiol can attenuate these AGE-mediated effects, suggesting that redox-sensitive signal transduction pathways are involved. Furthermore, these compounds may offer unique therapeutic opportunities for a successful anti-inflammatory and neuroprotective treatment of Alzheimer's disease.

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