Altered Calcium Homeostasis and Mitochondrial Dysfunction in Cortical Synaptic Compartments of Presenilin‐1 Mutant Mice
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M. Mattson | K. Duff | Sic L. Chan | W. Duan | J. Begley | Karen Duff
[1] M. Mattson,et al. Increased vulnerability of hippocampal neurons from presenilin-1 mutant knock-in mice to amyloid beta-peptide toxicity: central roles of superoxide production and caspase activation. , 2008, Journal of neurochemistry.
[2] M. Mattson,et al. Pivotal Role of Mitochondrial Calcium Uptake in Neural Cell Apoptosis and Necrosis , 1999, Journal of neurochemistry.
[3] M. Mattson,et al. Amyloid β-peptide induces apoptosis-related events in synapses and dendrites , 1998, Brain Research.
[4] M. Mattson,et al. Evidence for Synaptic Apoptosis , 1998, Experimental Neurology.
[5] M. Mattson,et al. Par-4 is a mediator of neuronal degeneration associated with the pathogenesis of Alzheimer disease , 1998, Nature Medicine.
[6] L. Oliver,et al. Induction of a Caspase-3-like Activity by Calcium in Normal Cytosolic Extracts Triggers Nuclear Apoptosis in a Cell-free System* , 1998, The Journal of Biological Chemistry.
[7] M. Mattson,et al. Increased Sensitivity to Mitochondrial Toxin-Induced Apoptosis in Neural Cells Expressing Mutant Presenilin-1 Is Linked to Perturbed Calcium Homeostasis and Enhanced Oxyradical Production , 1998, The Journal of Neuroscience.
[8] G. Schellenberg,et al. Presenilin‐1 mutation alters NGF‐induced neurite outgrowth, calcium homeostasis, and transcription factor (AP‐1) activation in PC12 cells , 1998, Journal of neuroscience research.
[9] M. Mattson,et al. Secreted β-Amyloid Precursor Protein Counteracts the Proapoptotic Action of Mutant Presenilin-1 by Activation of NF-κB and Stabilization of Calcium Homeostasis* , 1998, The Journal of Biological Chemistry.
[10] C. Haass,et al. Proteolytic fragments of the Alzheimer's disease associated presenilins-1 and -2 are phosphorylated in vivo by distinct cellular mechanisms. , 1998, Biochemistry.
[11] M. Mattson,et al. Calbindin D28k blocks the proapoptotic actions of mutant presenilin 1: reduced oxidative stress and preserved mitochondrial function. , 1998, Proceedings of the National Academy of Sciences of the United States of America.
[12] Gurparkash Singh,et al. Mutant Human Presenilin 1 Protects presenilin 1 Null Mouse against Embryonic Lethality and Elevates Aβ1–42/43 Expression , 1998, Neuron.
[13] D. Borchelt,et al. An Alzheimer's Disease-Linked PS1 Variant Rescues the Developmental Abnormalities of PS1-Deficient Embryos , 1998, Neuron.
[14] M. Mattson,et al. Calcium and reactive oxygen species mediate staurosporine‐induced mitochondrial dysfunction and apoptosis in PC12 cells , 1998, Journal of neuroscience research.
[15] J. B. Hutchins,et al. Mitochondrial Manganese Superoxide Dismutase Prevents Neural Apoptosis and Reduces Ischemic Brain Injury: Suppression of Peroxynitrite Production, Lipid Peroxidation, and Mitochondrial Dysfunction , 1998, The Journal of Neuroscience.
[16] M. Mattson,et al. Presenilins, the Endoplasmic Reticulum, and Neuronal Apoptosis in Alzheimer's Disease , 1998, Journal of neurochemistry.
[17] F. Checler,et al. α‐Secretase‐Derived Product of β‐Amyloid Precursor Protein Is Decreased by Presenilin 1 Mutations Linked to Familial Alzheimer's Disease , 1997 .
[18] T. Takadera,et al. Apoptotic cell death and caspase 3 (CPP32) activation induced by calcium ionophore at low concentrations and their prevention by nerve growth factor in PC12 cells. , 1997, European journal of biochemistry.
[19] Rudolph E Tanzi,et al. Presenilins and Alzheimer's disease , 1997, Current Opinion in Neurobiology.
[20] B. K. Hartman,et al. Nerve Growth Factor-independent Reduction in Choline Acetyltransferase Activity in PC12 Cells Expressing Mutant Presenilin-1* , 1997, The Journal of Biological Chemistry.
[21] D. Selkoe,et al. Interaction between amyloid precursor protein and presenilins in mammalian cells: implications for the pathogenesis of Alzheimer disease. , 1997, Proceedings of the National Academy of Sciences of the United States of America.
[22] 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.
[23] M. Mattson,et al. Alzheimer’s Presenilin Mutation Sensitizes Neural Cells to Apoptosis Induced by Trophic Factor Withdrawal and Amyloid β-Peptide: Involvement of Calcium and Oxyradicals , 1997, The Journal of Neuroscience.
[24] S. Tonegawa,et al. Skeletal and CNS Defects in Presenilin-1-Deficient Mice , 1997, Cell.
[25] D. Price,et al. Presenilin 1 is required for Notch 1 and Dll1 expression in the paraxial mesoderm , 1997, Nature.
[26] M. Mattson,et al. Basic FGF attenuates amyloid β-peptide-induced oxidative stress, mitochondrial dysfunction, and impairment of Na+/K+-ATPase activity in hippocampal neurons , 1997, Brain Research.
[27] M. Hoth,et al. Mitochondrial Regulation of Store-operated Calcium Signaling in T Lymphocytes , 1997, The Journal of cell biology.
[28] D. Harris,et al. Evidence for a Six-transmembrane Domain Structure of Presenilin 1* , 1997, The Journal of Biological Chemistry.
[29] John Hardy,et al. Amyloid, the presenilins and Alzheimer's disease , 1997, Trends in Neurosciences.
[30] K. Beyreuther,et al. Formation of stable complexes between two Alzheimer's disease gene products: Presenilin-2 and β-amyloid precursor protein , 1997, Nature Medicine.
[31] P. S. St George-Hyslop,et al. Phosphorylation, Subcellular Localization, and Membrane Orientation of the Alzheimer's Disease-associated Presenilins* , 1997, The Journal of Biological Chemistry.
[32] M. Mattson,et al. A Role for 4‐Hydroxynonenal, an Aldehydic Product of Lipid Peroxidation, in Disruption of Ion Homeostasis and Neuronal Death Induced by Amyloid β‐Peptide , 1997, Journal of neurochemistry.
[33] K M Harris,et al. Three-Dimensional Organization of Smooth Endoplasmic Reticulum in Hippocampal CA1 Dendrites and Dendritic Spines of the Immature and Mature Rat , 1997, The Journal of Neuroscience.
[34] M. Mattson,et al. Alzheimer's PS‐1 mutation perturbs calcium homeostasis and sensitizes PC12 cells to death induced by amyloid β‐peptide , 1996, Neuroreport.
[35] D. Selkoe,et al. The Alzheimer’s Disease-Associated Presenilins Are Differentially Phosphorylated Proteins Located Predominantly within the Endoplasmic Reticulum , 1996, Molecular medicine.
[36] M. Mattson,et al. Increased Activity‐Regulating and Neuroprotective Efficacy of α‐Secretase‐Derived Secreted Amyloid Precursor Protein Conferred by a C‐Terminal Heparin‐Binding Domain , 1996, Journal of neurochemistry.
[37] Allan I. Levey,et al. Familial Alzheimer's Disease–Linked Presenilin 1 Variants Elevate Aβ1–42/1–40 Ratio In Vitro and In Vivo , 1996, Neuron.
[38] D. Borchelt,et al. Protein Topology of Presenilin 1 , 1996, Neuron.
[39] J. Hardy,et al. Increased amyloid-β42(43) in brains of mice expressing mutant presenilin 1 , 1996, Nature.
[40] T. Sunderland,et al. Physiologic Levels of β‐Amyloid Activate Phosphatidylinositol 3‐Kinase with the Involvement of Tyrosine Phosphorylation , 1996, Journal of neurochemistry.
[41] J. Trojanowski,et al. Expression and analysis of presenilin 1 in a human neuronal system: localization in cell bodies and dendrites. , 1996, Proceedings of the National Academy of Sciences of the United States of America.
[42] J. Shioi,et al. Identification and neuron specific expression of the S182/presenilin I protein in human and rodent brains , 1996 .
[43] G. Schellenberg,et al. Secreted amyloid β–protein similar to that in the senile plaques of Alzheimer's disease is increased in vivo by the presenilin 1 and 2 and APP mutations linked to familial Alzheimer's disease , 1996, Nature Medicine.
[44] J. Blusztajn,et al. Amyloid beta-protein reduces acetylcholine synthesis in a cell line derived from cholinergic neurons of the basal forebrain. , 1996, Proceedings of the National Academy of Sciences of the United States of America.
[45] K. Imahori,et al. Characterization of human presenilin 1 using N‐terminal specific monoclonal antibodies: Evidence that Alzheimer mutations affect proteolytic processing , 1996, FEBS letters.
[46] D. Borchelt,et al. Endoproteolysis of Presenilin 1 and Accumulation of Processed Derivatives In Vivo , 1996, Neuron.
[47] B. Yankner. Mechanisms of Neuronal Degeneration in Alzheimer's Disease , 1996, Neuron.
[48] B. Hyman,et al. Alzheimer–associated presenilins 1 and 2 : Neuronal expression in brain and localization to intracellular membranes in mammalian cells , 1996, Nature Medicine.
[49] I. Kaneko,et al. Suppression of Mitochondrial Succinate Dehydrogenase, a Primary Target of β‐Amyloid, and Its Derivative Racemized at Ser Residue , 1995, Journal of neurochemistry.
[50] Iva Greenwald,et al. Facilitation of lin-12-mediated signalling by sel-12, a Caenorhabditis elegans S182 Alzheimer's disease gene , 1995, Nature.
[51] M. Beal,et al. Aging, energy, and oxidative stress in neurodegenerative diseases , 1995, Annals of neurology.
[52] M. Mattson,et al. Amyloid beta-peptide impairs ion-motive ATPase activities: evidence for a role in loss of neuronal Ca2+ homeostasis and cell death , 1995, The Journal of neuroscience : the official journal of the Society for Neuroscience.
[53] S. Rapoport,et al. β-Amyloid polypeptide increases calcium-uptake in PC12 cells: a possible mechanism for its cellular toxicity in Alzheimer's disease , 1994, Brain Research.
[54] T B Shea,et al. Calcium‐Activated Neutral Proteinase (Calpain) System in Aging and Alzheimer's Disease a , 1994, Annals of the New York Academy of Sciences.
[55] M. Mattson,et al. Secreted Forms of β-Amyloid Precursor Protein Protect Hippocampal Neurons against Amyloid β-Peptide-Induced Oxidative Injury , 1994, Experimental Neurology.
[56] K. Oka,et al. Internal Ca2+ mobilization is altered in fibroblasts from patients with Alzheimer disease. , 1994, Proceedings of the National Academy of Sciences of the United States of America.
[57] B. Hyman,et al. Neurochemical and histologic characterization of striatal excitotoxic lesions produced by the mitochondrial toxin 3-nitropropionic acid , 1993, The Journal of neuroscience : the official journal of the Society for Neuroscience.
[58] M. Mattson,et al. Calcium-destabilizing and neurodegenerative effects of aggregated β-amyloid peptide are attenuated by basic FGF , 1993, Brain Research.
[59] K. Jellinger,et al. Synaptic Pathology of Alzheimer's Disease a , 1993, Annals of the New York Academy of Sciences.
[60] 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.
[61] M. Mattson,et al. Evidence for excitoprotective and intraneuronal calcium-regulating roles for secreted forms of the β-amyloid precursor protein , 1993, Neuron.
[62] M. Mattson,et al. beta-Amyloid peptides destabilize calcium homeostasis and render human cortical neurons vulnerable to excitotoxicity , 1992, The Journal of neuroscience : the official journal of the Society for Neuroscience.
[63] C. Cotman,et al. β-Amyloid protein increases the vulnerability of cultured cortical neurons to excitotoxic damage , 1990, Brain Research.
[64] G. Pepeu,et al. Effect of Age on K+‐Induced Cytosolic Ca2+ Changes in Rat Cortical Synaptosomes , 1989, Journal of neurochemistry.
[65] P. Gordon-Weeks,et al. Presynaptic microtubules: Organisation and assembly/disassembly , 1982, Neuroscience.
[66] C. Cotman,et al. Synaptic plasma membranes from rat brain synaptosomes: isolation and partial characterization. , 1971, Biochimica et biophysica acta.
[67] Miles W. Miller,et al. Increased vulnerability of hippocampal neurons to excitotoxic necrosis in presenilin-1 mutant knock-in mice , 1999, Nature Medicine.
[68] Weiming Xia,et al. Mutant presenilins of Alzheimer's disease increase production of 42-residue amyloid β-protein in both transfected cells and transgenic mice , 1997, Nature Medicine.
[69] M. Mattson,et al. Calcium Homeostasis and Free Radical Metabolism as Convergence Points in the Pathophysiology of Dementia , 1997 .
[70] J. Shioi,et al. Identification and neuron specific expression of the S182/presenilin I protein in human and rodent brains. , 1996, Journal of neuroscience research.
[71] H. Mantsch,et al. Human and rodent Alzheimer beta-amyloid peptides acquire distinct conformations in membrane-mimicking solvents. , 1993, European journal of biochemistry.