Increased mtDNA mutations with aging promotes amyloid accumulation and brain atrophy in the APP/Ld transgenic mouse model of Alzheimer’s disease
暂无分享,去创建一个
[1] Brian J. Bacskai,et al. Mitochondrial Alterations near Amyloid Plaques in an Alzheimer's Disease Mouse Model , 2013, The Journal of Neuroscience.
[2] W. Klein. Synaptotoxic amyloid-β oligomers: a molecular basis for the cause, diagnosis, and treatment of Alzheimer's disease? , 2012, Journal of Alzheimer's disease : JAD.
[3] R. Vassar,et al. Neuron loss in the 5XFAD mouse model of Alzheimer’s disease correlates with intraneuronal Aβ42 accumulation and Caspase-3 activation , 2013, Molecular Neurodegeneration.
[4] R. Tanzi. The genetics of Alzheimer disease. , 2012, Cold Spring Harbor perspectives in medicine.
[5] T. Prolla,et al. Increased mitochondrial biogenesis in muscle improves aging phenotypes in the mtDNA mutator mouse. , 2012, Human molecular genetics.
[6] R. Vassar,et al. Cdk5 Protein Inhibition and Aβ42 Increase BACE1 Protein Level in Primary Neurons by a Post-transcriptional Mechanism , 2012, The Journal of Biological Chemistry.
[7] 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.
[8] P. Gean,et al. The Involvement of Cdk5 Activator p35 in Social Isolation-Triggered Onset of Early Alzheimer’s Disease-Related Cognitive Deficit in the Transgenic Mice , 2011, Neuropsychopharmacology.
[9] M. Lambert,et al. Intraneuronal amyloid-beta oligomers cause cell death via endoplasmic reticulum stress, endosomal/lysosomal leakage, and mitochondrial dysfunction in vivo , 2011, Alzheimer's & Dementia.
[10] W. Klein,et al. Intraneuronal amyloid β oligomers cause cell death via endoplasmic reticulum stress, endosomal/lysosomal leakage, and mitochondrial dysfunction in vivo , 2011, Journal of neuroscience research.
[11] P. Reddy,et al. Impaired mitochondrial dynamics and abnormal interaction of amyloid beta with mitochondrial protein Drp1 in neurons from patients with Alzheimer's disease: implications for neuronal damage. , 2011, Human molecular genetics.
[12] T. Prolla,et al. Mitochondrial DNA polymerase editing mutation, PolgD257A, reduces the diabetic phenotype of Akita male mice by suppressing appetite , 2011, Proceedings of the National Academy of Sciences.
[13] Gregory C Kujoth,et al. Endurance exercise rescues progeroid aging and induces systemic mitochondrial rejuvenation in mtDNA mutator mice , 2011, Proceedings of the National Academy of Sciences.
[14] A. Bacci,et al. Caspase-3 triggers early synaptic dysfunction in a mouse model of Alzheimer's disease , 2011, Nature Neuroscience.
[15] T. Prolla,et al. The mtDNA mutation spectrum of the progeroid Polg mutator mouse includes abundant control region multimers. , 2010, Cell metabolism.
[16] Takuya Miyakawa,et al. Mitochondrial DNA Mutations Induce Mitochondrial Dysfunction, Apoptosis and Sarcopenia in Skeletal Muscle of Mitochondrial DNA Mutator Mice , 2010, PloS one.
[17] R. Swerdlow,et al. The Alzheimer's disease mitochondrial cascade hypothesis. , 2010, Journal of Alzheimer's disease : JAD.
[18] B. Yankner,et al. Neural mechanisms of ageing and cognitive decline , 2010, Nature.
[19] Jan Nedergaard,et al. Random point mutations with major effects on protein-coding genes are the driving force behind premature aging in mtDNA mutator mice. , 2009, Cell metabolism.
[20] T. Prolla,et al. Mice expressing an error-prone DNA polymerase in mitochondria display elevated replication pausing and chromosomal breakage at fragile sites of mitochondrial DNA , 2009, Nucleic acids research.
[21] Xiongwei Zhu,et al. Amyloid-β overproduction causes abnormal mitochondrial dynamics via differential modulation of mitochondrial fission/fusion proteins , 2008, Proceedings of the National Academy of Sciences.
[22] 福家 聡,et al. DNA deletions and clonal mutations drive premature aging in mitochondrial mutator mice , 2008 .
[23] R. Nixon,et al. Neuronal apoptosis and autophagy cross talk in aging PS/APP mice, a model of Alzheimer's disease. , 2008, American Journal of Pathology.
[24] H. Tanila,et al. Increased expression of Aβ degrading enzyme IDE in the cortex of transgenic mice with Alzheimer's disease-like neuropathology , 2008, Neuroscience Letters.
[25] E. Head,et al. Caspase Activation in Alzheimer's Disease: Early to Rise and Late to Bed , 2008, Reviews in the neurosciences.
[26] R. Berry,et al. β-Site Amyloid Precursor Protein Cleaving Enzyme 1 Levels Become Elevated in Neurons around Amyloid Plaques: Implications for Alzheimer's Disease Pathogenesis , 2007, The Journal of Neuroscience.
[27] M. Ohno,et al. BACE1 gene deletion prevents neuron loss and memory deficits in 5XFAD APP/PS1 transgenic mice , 2007, Neurobiology of Disease.
[28] T. Prolla,et al. The Role of Mitochondrial DNA Mutations in Mammalian Aging , 2007, PLoS genetics.
[29] R. Berry,et al. Beta-site amyloid precursor protein cleaving enzyme 1 levels become elevated in neurons around amyloid plaques: implications for Alzheimer's disease pathogenesis. , 2007, The Journal of neuroscience : the official journal of the Society for Neuroscience.
[30] M. Ohno,et al. Intraneuronal β-Amyloid Aggregates, Neurodegeneration, and Neuron Loss in Transgenic Mice with Five Familial Alzheimer's Disease Mutations: Potential Factors in Amyloid Plaque Formation , 2006, The Journal of Neuroscience.
[31] E. Sigurdsson,et al. Plaque-Associated Overexpression of Insulin-Degrading Enzyme in the Cerebral Cortex of Aged Transgenic Tg2576 Mice With Alzheimer Pathology , 2006, Journal of neuropathology and experimental neurology.
[32] J. Quinn,et al. Mitochondria are a direct site of A beta accumulation in Alzheimer's disease neurons: implications for free radical generation and oxidative damage in disease progression. , 2006, Human molecular genetics.
[33] Stavros J. Baloyannis,et al. Mitochondrial alterations in Alzheimer's disease. , 2006, Journal of Alzheimer's disease : JAD.
[34] A. LeBlanc,et al. The role of apoptotic pathways in Alzheimer's disease neurodegeneration and cell death. , 2005, Current Alzheimer research.
[35] T. D. Pugh,et al. Mitochondrial DNA Mutations, Oxidative Stress, and Apoptosis in Mammalian Aging , 2005, Science.
[36] Yama Akbari,et al. Age- and region-dependent alterations in Aβ-degrading enzymes: implications for Aβ-induced disorders , 2005, Neurobiology of Aging.
[37] R. Tanzi,et al. Twenty Years of the Alzheimer’s Disease Amyloid Hypothesis: A Genetic Perspective , 2005, Cell.
[38] Yama Akbari,et al. Age- and region-dependent alterations in Abeta-degrading enzymes: implications for Abeta-induced disorders. , 2005, Neurobiology of aging.
[39] C. Broeckhoven,et al. POLG mutations in neurodegenerative disorders with ataxia but no muscle involvement , 2004, Neurology.
[40] Li-Huei Tsai,et al. Cdk5 deregulation in the pathogenesis of Alzheimer's disease. , 2004, Trends in molecular medicine.
[41] Howard T. Jacobs,et al. Premature ageing in mice expressing defective mitochondrial DNA polymerase , 2004, Nature.
[42] K. Duff,et al. Transgenic mouse models of Alzheimer's disease: how useful have they been for therapeutic development? , 2004, Briefings in functional genomics & proteomics.
[43] M. Duchen,et al. β-Amyloid Peptides Induce Mitochondrial Dysfunction and Oxidative Stress in Astrocytes and Death of Neurons through Activation of NADPH Oxidase , 2004, The Journal of Neuroscience.
[44] J. Troncoso,et al. Caspase activation in the limbic cortex of subjects with early Alzheimer's disease , 2003, Annals of neurology.
[45] L. Hersh,et al. Amyloid-β peptide levels in brain are inversely correlated with insulysin activity levels in vivo , 2003, Proceedings of the National Academy of Sciences of the United States of America.
[46] Matthew P. Frosch,et al. Insulin-degrading enzyme regulates the levels of insulin, amyloid β-protein, and the β-amyloid precursor protein intracellular domain in vivo , 2003, Proceedings of the National Academy of Sciences of the United States of America.
[47] D. Selkoe,et al. Insulin-degrading enzyme regulates the levels of insulin, amyloid beta-protein, and the beta-amyloid precursor protein intracellular domain in vivo. , 2003, Proceedings of the National Academy of Sciences of the United States of America.
[48] Y. Suh,et al. Amyloid &bgr; peptide induces cytochrome c release from isolated mitochondria , 2002, Neuroreport.
[49] H. Cuckle,et al. Mitochondrial dysfunction and Down's syndrome. , 2002, BioEssays : news and reviews in molecular, cellular and developmental biology.
[50] Dae-Yeop Hwang,et al. Alterations in behavior, amyloid p‐42, caspase‐3, and Cox‐2 in mutant PS2 transgenic mouse model of Alzheimer's disease , 2002, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.
[51] Sangram S. Sisodia,et al. γ-Secretase, notch, Aβ and alzheimer's disease: Where do the presenilins fit in? , 2002, Nature Reviews Neuroscience.
[52] P. S. St George-Hyslop,et al. gamma-Secretase, Notch, Abeta and Alzheimer's disease: where do the presenilins fit in? , 2002, Nature reviews. Neuroscience.
[53] T. Saido,et al. Metabolic Regulation of Brain Aβ by Neprilysin , 2001, Science.
[54] Carl W. Cotman,et al. Activated caspase-3 expression in Alzheimer’s and aged control brain: correlation with Alzheimer pathology , 2001, Brain Research.
[55] D. Selkoe. Alzheimer's disease: genes, proteins, and therapy. , 2001, Physiological reviews.
[56] Colin Adrain,et al. Executioner Caspase-3, -6, and -7 Perform Distinct, Non-redundant Roles during the Demolition Phase of Apoptosis* , 2001, The Journal of Biological Chemistry.
[57] W. Richards,et al. Mice deficient in BACE1, the Alzheimer's β-secretase, have normal phenotype and abolished β-amyloid generation , 2001, Nature Neuroscience.
[58] H. Cai,et al. BACE1 is the major beta-secretase for generation of Abeta peptides by neurons. , 2001, Nature neuroscience.
[59] W. Richards,et al. Mice deficient in BACE1, the Alzheimer's beta-secretase, have normal phenotype and abolished beta-amyloid generation. , 2001, Nature neuroscience.
[60] T. Saido,et al. Metabolic regulation of brain Abeta by neprilysin. , 2001, Science.
[61] I. Tesseur,et al. Modeling Alzheimer's disease in transgenic mice: effect of age and of Presenilin1 on amyloid biochemistry and pathology in APP/London mice , 2000, Experimental Gerontology.
[62] J. Tang,et al. Human aspartic protease memapsin 2 cleaves the beta-secretase site of beta-amyloid precursor protein. , 2000, Proceedings of the National Academy of Sciences of the United States of America.
[63] C. Behl,et al. Apoptosis and Alzheimer's disease , 2000, Journal of Neural Transmission.
[64] Alfredo G. Tomasselli,et al. Membrane-anchored aspartyl protease with Alzheimer's disease β-secretase activity , 1999, Nature.
[65] R. Barbour,et al. Purification and cloning of amyloid precursor protein β-secretase from human brain , 1999, Nature.
[66] J. Treanor,et al. Beta-secretase cleavage of Alzheimer's amyloid precursor protein by the transmembrane aspartic protease BACE. , 1999, Science.
[67] David Smith,et al. Involvement of Caspases in Proteolytic Cleavage of Alzheimer’s Amyloid-β Precursor Protein and Amyloidogenic Aβ Peptide Formation , 1999, Cell.
[68] Veerle Baekelandt,et al. Early Phenotypic Changes in Transgenic Mice That Overexpress Different Mutants of Amyloid Precursor Protein in Brain* , 1999, The Journal of Biological Chemistry.
[69] G. Robertson,et al. Involvement of caspases in proteolytic cleavage of Alzheimer's amyloid-beta precursor protein and amyloidogenic A beta peptide formation. , 1999, Cell.
[70] C. Southan,et al. Identification of a novel aspartic protease (Asp 2) as beta-secretase. , 1999, Molecular and cellular neurosciences.
[71] L. Hersh,et al. Insulin-degrading Enzyme Regulates Extracellular Levels of Amyloid β-Protein by Degradation* , 1998, The Journal of Biological Chemistry.
[72] C. Geula,et al. Aging renders the brain vulnerable to amyloid beta-protein neurotoxicity. , 1998, Nature medicine.
[73] M. Mattson,et al. Impairment of Glucose and Glutamate Transport and Induction of Mitochondrial Oxidative Stress and Dysfunction in Synaptosomes by Amyloid β‐Peptide: Role of the Lipid Peroxidation Product 4‐Hydroxynonenal , 1997, Journal of neurochemistry.
[74] M. Beal,et al. Marked changes in mitochondrial DNA deletion levels in Alzheimer brains. , 1994, Genomics.
[75] Kevin Cox,et al. Quantitative analysis of a vulnerable subset of pyramidal neurons in Alzheimer's disease: I. Superior frontal and inferior temporal cortex , 1990, The Journal of comparative neurology.