Aβ25–35 Suppresses Mitochondrial Biogenesis in Primary Hippocampal Neurons
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[1] K. Kuča,et al. A Direct Interaction Between Mitochondrial Proteins and Amyloid-β Peptide and its Significance for the Progression and Treatment of Alzheimer’s Disease , 2015, Current medicinal chemistry.
[2] G. Casadesus,et al. Early alterations in energy metabolism in the hippocampus of APPswe/PS1dE9 mouse model of Alzheimer's disease. , 2014, Biochimica et biophysica acta.
[3] A. Martínez-Amat,et al. The combination of oral quercetin supplementation and exercise prevents brain mitochondrial biogenesis , 2014, Genes & Nutrition.
[4] Xinglong Wang,et al. Oxidative stress and mitochondrial dysfunction in Alzheimer's disease. , 2014, Biochimica et biophysica acta.
[5] N. Jia,et al. Taurine attenuates amyloid β 1-42-induced mitochondrial dysfunction by activating of SIRT1 in SK-N-SH cells. , 2014, Biochemical and biophysical research communications.
[6] Yanzhuang Wang,et al. Aβ-induced Golgi fragmentation in Alzheimer’s disease enhances Aβ production , 2014, Proceedings of the National Academy of Sciences.
[7] F. Khodagholi,et al. Monitoring of Neuronal Loss in the Hippocampus of Aβ-Injected Rat: Autophagy, Mitophagy, and Mitochondrial Biogenesis Stand Against Apoptosis , 2014, NeuroMolecular Medicine.
[8] Brian J. Bacskai,et al. Mitochondrial Alterations near Amyloid Plaques in an Alzheimer's Disease Mouse Model , 2013, The Journal of Neuroscience.
[9] J. Prehn,et al. Bmf upregulation through the AMP-activated protein kinase pathway may protect the brain from seizure-induced cell death , 2013, Cell Death and Disease.
[10] Young Woo Kim,et al. Red ginseng abrogates oxidative stress via mitochondria protection mediated by LKB1-AMPK pathway , 2013, BMC Complementary and Alternative Medicine.
[11] D. Brautigan,et al. α–SNAP inhibits AMPK signaling to reduce mitochondrial biogenesis and dephosphorylates Thr172 in AMPKα in vitro , 2013, Nature Communications.
[12] K. Lim,et al. AMP Kinase Activation Mitigates Dopaminergic Dysfunction and Mitochondrial Abnormalities in Drosophila Models of Parkinson's Disease , 2012, The Journal of Neuroscience.
[13] R. de Cabo,et al. SIRT1 is required for AMPK activation and the beneficial effects of resveratrol on mitochondrial function. , 2012, Cell metabolism.
[14] I. Mook‐Jung,et al. Mitochondria-Specific Accumulation of Amyloid β Induces Mitochondrial Dysfunction Leading to Apoptotic Cell Death , 2012, PloS one.
[15] Hyoung-Gon Lee,et al. Impaired mitochondrial biogenesis contributes to mitochondrial dysfunction in Alzheimer’s disease , 2012, Journal of neurochemistry.
[16] G. Brooks,et al. Mild heat stress induces mitochondrial biogenesis in C2C12 myotubes. , 2012, Journal of applied physiology.
[17] P. Reddy,et al. Impaired mitochondrial biogenesis, defective axonal transport of mitochondria, abnormal mitochondrial dynamics and synaptic degeneration in a mouse model of Alzheimer's disease. , 2011, Human molecular genetics.
[18] R. Scarpulla,et al. Metabolic control of mitochondrial biogenesis through the PGC-1 family regulatory network. , 2011, Biochimica et biophysica acta.
[19] Z. Quezado,et al. Disruption of adaptive energy metabolism and elevated ribosomal p-S6K1 levels contribute to INCL pathogenesis: partial rescue by resveratrol. , 2011, Human molecular genetics.
[20] Jürgen Götz,et al. Amyloid-β and tau — a toxic pas de deux in Alzheimer's disease , 2011, Nature Reviews Neuroscience.
[21] Ezzie Hutchinson,et al. Systems neuroscience: The stress of dieting , 2011, Nature Reviews Neuroscience.
[22] S. Rohrbach,et al. Mitochondrial Biogenesis and Peroxisome Proliferator–Activated Receptor-γ Coactivator-1α (PGC-1α) Deacetylation by Physical Activity , 2010, Diabetes.
[23] S. Rohrbach,et al. Mitochondrial Biogenesis and Peroxisome Proliferator–Activated Receptor-γ Coactivator-1α (PGC-1α) Deacetylation by Physical Activity , 2010, Diabetes.
[24] P. Griffin,et al. Faculty Opinions recommendation of Fibroblast growth factor 21 regulates energy metabolism by activating the AMPK-SIRT1-PGC-1alpha pathway. , 2010 .
[25] Qing Yang,et al. Fibroblast growth factor 21 regulates energy metabolism by activating the AMPK–SIRT1–PGC-1α pathway , 2010, Proceedings of the National Academy of Sciences.
[26] N. Ruderman,et al. AMPK and SIRT1: a long-standing partnership? , 2010, American journal of physiology. Endocrinology and metabolism.
[27] W. Fan,et al. Differential effects of melatonin on amyloid‐β peptide 25–35‐induced mitochondrial dysfunction in hippocampal neurons at different stages of culture , 2010, Journal of pineal research.
[28] E. Kosenko,et al. Subcellular and metabolic examination of amyloid-β peptides in Alzheimer disease pathogenesis: Evidence for Aβ25–35 , 2010, Experimental Neurology.
[29] I. Cho,et al. Resveratrol Protects Mitochondria against Oxidative Stress through AMP-Activated Protein Kinase-Mediated Glycogen Synthase Kinase-3β Inhibition Downstream of Poly(ADP-ribose)polymerase-LKB1 Pathway , 2009, Molecular Pharmacology.
[30] P. Puigserver,et al. AMPK regulates energy expenditure by modulating NAD+ metabolism and SIRT1 activity , 2009, Nature.
[31] P. Filipcik,et al. Cortical and Hippocampal Neurons from Truncated Tau Transgenic Rat Express Multiple Markers of Neurodegeneration , 2009, Cellular and Molecular Neurobiology.
[32] J. Buxbaum,et al. PGC-1alpha expression decreases in the Alzheimer disease brain as a function of dementia. , 2009, Archives of neurology.
[33] M. Masserini,et al. TrkA pathway activation induced by amyloid-beta (Abeta) , 2009, Molecular and Cellular Neuroscience.
[34] D. Bennett,et al. Sirtuin 1 Reduction Parallels the Accumulation of Tau in Alzheimer Disease , 2009, Journal of neuropathology and experimental neurology.
[35] V. Sartorelli,et al. Comparing and contrasting the roles of AMPK and SIRT1 in metabolic tissues , 2008, Cell cycle.
[36] M. Ott,et al. The ups and downs of SIRT1. , 2008, Trends in biochemical sciences.
[37] G. McKhann,et al. Cyclophilin D deficiency attenuates mitochondrial and neuronal perturbation and ameliorates learning and memory in Alzheimer's disease , 2008, Nature Medicine.
[38] F. Mouliere,et al. Protective effect of BDNF against beta-amyloid induced neurotoxicity in vitro and in vivo in rats , 2008, Neurobiology of Disease.
[39] E. Hoffman,et al. Glucose restriction inhibits skeletal myoblast differentiation by activating SIRT1 through AMPK-mediated regulation of Nampt. , 2008, Developmental cell.
[40] D. Hardie,et al. AMP-activated/SNF1 protein kinases: conserved guardians of cellular energy , 2007, Nature Reviews Molecular Cell Biology.
[41] B. Spiegelman,et al. AMP-activated protein kinase (AMPK) action in skeletal muscle via direct phosphorylation of PGC-1α , 2007, Proceedings of the National Academy of Sciences.
[42] Andre Fischer,et al. SIRT1 deacetylase protects against neurodegeneration in models for Alzheimer's disease and amyotrophic lateral sclerosis , 2007, The EMBO journal.
[43] B. Spiegelman,et al. A fundamental system of cellular energy homeostasis regulated by PGC-1α , 2007, Proceedings of the National Academy of Sciences.
[44] P. Agostinho,et al. Susceptibility of hippocampal neurons to Aβ peptide toxicity is associated with perturbation of Ca2+ homeostasis , 2007, Brain Research.
[45] P. Puigserver,et al. Metabolic control of muscle mitochondrial function and fatty acid oxidation through SIRT1/PGC‐1α , 2007, The EMBO journal.
[46] J. Busciglio,et al. Different Conformations of Amyloid β Induce Neurotoxicity by Distinct Mechanisms in Human Cortical Neurons , 2006, The Journal of Neuroscience.
[47] Christoph Handschin,et al. Metabolic control through the PGC-1 family of transcription coactivators. , 2005, Cell metabolism.
[48] S. Nemoto,et al. SIRT1 Functionally Interacts with the Metabolic Regulator and Transcriptional Coactivator PGC-1α* , 2005, Journal of Biological Chemistry.
[49] D. Selkoe,et al. Cell biology of protein misfolding: The examples of Alzheimer's and Parkinson's diseases , 2004, Nature Cell Biology.
[50] M. Meselhy,et al. Aβ(25–35)-Induced Memory Impairment, Axonal Atrophy, and Synaptic Loss are Ameliorated by M1, A Metabolite of Protopanaxadiol-Type Saponins , 2004, Neuropsychopharmacology.
[51] Douglas L. Rothman,et al. Mitochondrial Dysfunction in the Elderly: Possible Role in Insulin Resistance , 2003, Science.
[52] M. Duchen,et al. β-Amyloid Fragment 25–35 Causes Mitochondrial Dysfunction in Primary Cortical Neurons , 2002, Neurobiology of Disease.
[53] J. Hardy,et al. The Amyloid Hypothesis of Alzheimer ’ s Disease : Progress and Problems on the Road to Therapeutics , 2009 .
[54] Rick B. Vega,et al. The Coactivator PGC-1 Cooperates with Peroxisome Proliferator-Activated Receptor α in Transcriptional Control of Nuclear Genes Encoding Mitochondrial Fatty Acid Oxidation Enzymes , 2000, Molecular and Cellular Biology.
[55] T. Bates,et al. β‐Amyloid fragment 25–35 selectively decreases complex IV activity in isolated mitochondria , 1999, FEBS letters.
[56] V. Mootha,et al. Mechanisms Controlling Mitochondrial Biogenesis and Respiration through the Thermogenic Coactivator PGC-1 , 1999, Cell.
[57] R. Scarpulla,et al. Activation of the human mitochondrial transcription factor A gene by nuclear respiratory factors: a potential regulatory link between nuclear and mitochondrial gene expression in organelle biogenesis. , 1994, Proceedings of the National Academy of Sciences of the United States of America.
[58] Carl W. Cotman,et al. Neurodegeneration induced by beta-amyloid peptides in vitro: the role of peptide assembly state , 1993, The Journal of neuroscience : the official journal of the Society for Neuroscience.
[59] D. Kirschner,et al. Neurotrophic and neurotoxic effects of amyloid beta protein: reversal by tachykinin neuropeptides. , 1990, Science.
[60] T. Mosmann. Rapid colorimetric assay for cellular growth and survival: application to proliferation and cytotoxicity assays. , 1983, Journal of immunological methods.
[61] J. Bennett,et al. Mitochondrial DNA copy numbers in pyramidal neurons are decreased and mitochondrial biogenesis transcriptome signaling is disrupted in Alzheimer's disease hippocampi. , 2014, Journal of Alzheimer's disease : JAD.
[62] S. Yan,et al. Amyloid-beta-induced mitochondrial dysfunction. , 2007, Journal of Alzheimer's disease : JAD.
[63] B. Spiegelman,et al. AMP-activated protein kinase (AMPK) action in skeletal muscle via direct phosphorylation of PGC-1alpha. , 2007, Proceedings of the National Academy of Sciences of the United States of America.
[64] S. Yan,et al. Amyloid-β-Induced Mitochondrial Dysfunction , 2007 .
[65] Steven P Gygi,et al. Nutrient control of glucose homeostasis through a complex of PGC-1alpha and SIRT1. , 2005, Nature.
[66] M. Duchen,et al. Beta-amyloid fragment 25-35 causes mitochondrial dysfunction in primary cortical neurons. , 2002, Neurobiology of disease.