Laura Canevari

Summary

Affiliation: University College London
Country: UK

Publications

  1. ncbi request reprint beta-Amyloid fragment 25-35 selectively decreases complex IV activity in isolated mitochondria
    L Canevari
    Department of Neurochemistry, Institute of Neurology, London, UK
    FEBS Lett 457:131-4. 1999
  2. ncbi request reprint Toxicity of amyloid beta peptide: tales of calcium, mitochondria, and oxidative stress
    Laura Canevari
    Division of Neurochemistry, Institute of Neurology, Queen Square, London WC1N 3BG, United Kingdom
    Neurochem Res 29:637-50. 2004
  3. ncbi request reprint Calcium signals induced by amyloid beta peptide and their consequences in neurons and astrocytes in culture
    Andrey Y Abramov
    Department of Physiology, University College London, Gower Street WC1E 6BT, London, UK
    Biochim Biophys Acta 1742:81-7. 2004
  4. ncbi request reprint Alzheimer's disease and cholesterol: the fat connection
    Laura Canevari
    Miriam Marks Division of Neurochemistry, Department of Molecular Neuroscience, Institute of Neurology, University College London, Queen Square, London, UK
    Neurochem Res 32:739-50. 2007
  5. ncbi request reprint Changes in intracellular calcium and glutathione in astrocytes as the primary mechanism of amyloid neurotoxicity
    Andrey Y Abramov
    Mitochondrial Biology Group, Department of Physiology, University College London, London WC1E 6BT, United Kingdom
    J Neurosci 23:5088-95. 2003
  6. ncbi request reprint Beta-amyloid peptides induce mitochondrial dysfunction and oxidative stress in astrocytes and death of neurons through activation of NADPH oxidase
    Andrey Y Abramov
    Mitochondrial Biology Group, Department of Physiology, University College London, London WC1E 6BT, United Kingdom
    J Neurosci 24:565-75. 2004
  7. ncbi request reprint Lack of prion protein expression results in a neuronal phenotype sensitive to stress
    David R Brown
    Department of Biochemistry, Cambridge University, Cambridge, United Kingdom
    J Neurosci Res 67:211-24. 2002
  8. ncbi request reprint Nitric oxide and peroxynitrite cause irreversible increases in the K(m) for oxygen of mitochondrial cytochrome oxidase: in vitro and in vivo studies
    Chris E Cooper
    Department of Biological Sciences, University of Essex, Central Campus Wivenhoe Park, Essex CO4 3SQ, Colchester, UK
    Biochim Biophys Acta 1607:27-34. 2003
  9. ncbi request reprint Expression and modulation of an NADPH oxidase in mammalian astrocytes
    Andrey Y Abramov
    Department of Physiology, University College London, London WC1E 6BT, United Kingdom
    J Neurosci 25:9176-84. 2005

Detail Information

Publications9

  1. ncbi request reprint beta-Amyloid fragment 25-35 selectively decreases complex IV activity in isolated mitochondria
    L Canevari
    Department of Neurochemistry, Institute of Neurology, London, UK
    FEBS Lett 457:131-4. 1999
    ..The reverse sequence peptide (35-25) had no effect on any of the activities measured. We conclude that inhibition of mitochondrial complex IV might be a contributing factor to the pathogenesis of Alzheimer's disease...
  2. ncbi request reprint Toxicity of amyloid beta peptide: tales of calcium, mitochondria, and oxidative stress
    Laura Canevari
    Division of Neurochemistry, Institute of Neurology, Queen Square, London WC1N 3BG, United Kingdom
    Neurochem Res 29:637-50. 2004
    ..Studies in vitro also show alterations in cellular calcium signaling. We consider the mechanisms proposed to mediate cell injury and explore evidence to indicate which of these many changes in function are primary and which secondary...
  3. ncbi request reprint Calcium signals induced by amyloid beta peptide and their consequences in neurons and astrocytes in culture
    Andrey Y Abramov
    Department of Physiology, University College London, Gower Street WC1E 6BT, London, UK
    Biochim Biophys Acta 1742:81-7. 2004
    ..These data suggest that Abeta causes Ca(2+)-dependent oxidative stress by activating an astrocytic NADPH oxidase, and that neuronal death follows through a failure of antioxidant support...
  4. ncbi request reprint Alzheimer's disease and cholesterol: the fat connection
    Laura Canevari
    Miriam Marks Division of Neurochemistry, Department of Molecular Neuroscience, Institute of Neurology, University College London, Queen Square, London, UK
    Neurochem Res 32:739-50. 2007
    ..Finally, we report some of our results pointing at the interplay between neurons and astrocytes and NADPH oxidase activation as a new candidate mechanism linking cholesterol and AD pathology...
  5. ncbi request reprint Changes in intracellular calcium and glutathione in astrocytes as the primary mechanism of amyloid neurotoxicity
    Andrey Y Abramov
    Mitochondrial Biology Group, Department of Physiology, University College London, London WC1E 6BT, United Kingdom
    J Neurosci 23:5088-95. 2003
    ..Thus, astrocytes appear to be the primary target of betaA, whereas the neurotoxicity reflects the neuronal dependence on astrocytes for antioxidant support...
  6. ncbi request reprint Beta-amyloid peptides induce mitochondrial dysfunction and oxidative stress in astrocytes and death of neurons through activation of NADPH oxidase
    Andrey Y Abramov
    Mitochondrial Biology Group, Department of Physiology, University College London, London WC1E 6BT, United Kingdom
    J Neurosci 24:565-75. 2004
    ....
  7. ncbi request reprint Lack of prion protein expression results in a neuronal phenotype sensitive to stress
    David R Brown
    Department of Biochemistry, Cambridge University, Cambridge, United Kingdom
    J Neurosci Res 67:211-24. 2002
    ..The implication of these results is that the consequence of genetic ablation of genes must include biochemical analysis as well as analyses of possible developmental and behavioral changes...
  8. ncbi request reprint Nitric oxide and peroxynitrite cause irreversible increases in the K(m) for oxygen of mitochondrial cytochrome oxidase: in vitro and in vivo studies
    Chris E Cooper
    Department of Biological Sciences, University of Essex, Central Campus Wivenhoe Park, Essex CO4 3SQ, Colchester, UK
    Biochim Biophys Acta 1607:27-34. 2003
    ..Studies of cell respiration that fail to vary the oxygen concentration systematically are therefore likely to significantly underestimate the degree of irreversible damage to cytochrome oxidase...
  9. ncbi request reprint Expression and modulation of an NADPH oxidase in mammalian astrocytes
    Andrey Y Abramov
    Department of Physiology, University College London, London WC1E 6BT, United Kingdom
    J Neurosci 25:9176-84. 2005
    ..The astrocytic NADPH oxidase is likely to play important roles in CNS physiology and pathology...