Increased mtDNA mutations with aging promotes amyloid accumulation and brain atrophy in the APP/Ld transgenic mouse model of Alzheimer’s disease

[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.