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Adenosine Triphosphate, metabolism; Amyloid beta-Peptides, secretion; Amyloid beta-Protein Precursor, metabolism; Cell Line, Tumor; DNA, Mitochondrial, genetics; Electron Transport, drug effects; Electron Transport Chain Complex Proteins, metabolism; Ginkgo biloba, chemistry; Humans; Mitochondria, metabolism; Oxidative Phosphorylation, drug effects; Oxidative Stress, drug effects; Oxygen, metabolism; Plant Extracts, pharmacology; Reactive Oxygen Species, metabolism; Up-Regulation, drug effects
Abstract
Energy deficiency and mitochondrial failure have been recognized as a prominent, early event in Alzheimer's disease (AD). Recently, we demonstrated that chronic exposure to amyloid-beta (Abeta) in human neuroblastoma cells over-expressing human wild-type amyloid precursor protein (APP) resulted in (i) activity changes of complexes III and IV of the oxidative phosphorylation system (OXPHOS) and in (ii) a drop of ATP levels which may finally instigate loss of synapses and neuronal cell death in AD. Therefore, the aim of the present study was to investigate whether standardized Ginkgo biloba extract LI 1370 (GBE) is able to rescue Abeta-induced defects in energy metabolism.
