John M Land

Summary

Affiliation: University College London
Country: UK

Publications

  1. ncbi Some observations upon biochemical causes of ataxia and a new disease entity ubiquinone, CoQ10 deficiency
    John M Land
    Neurometabolic Unit Box 105, National Hospital for Neurology and Neurosurgery, Queen Square, London, WC1N 3BG, UK
    Neurochem Res 32:837-43. 2007
  2. ncbi The effect of HMG-CoA reductase inhibitors on coenzyme Q10: possible biochemical/clinical implications
    Iain P Hargreaves
    Neurometabolic Unit, National Hospital for Neurology and Neurosurgery, Queen Square, London WC1N 3BG, UK
    Drug Saf 28:659-76. 2005
  3. ncbi Determination of coenzyme Q10 status in blood mononuclear cells, skeletal muscle, and plasma by HPLC with di-propoxy-coenzyme Q10 as an internal standard
    Andrew J Duncan
    Division of Neurochemistry, Institute of Neurology, London, UK
    Clin Chem 51:2380-2. 2005
  4. ncbi Oxidative stress and mitochondrial dysfunction in neurodegeneration; cardiolipin a critical target?
    Simon Pope
    Neurometabolic Unit, National Hospital, UCLH Foundation Trust, UCL, Queen Square, London, WC1N 3BG, UK
    Biochim Biophys Acta 1777:794-9. 2008
  5. ncbi Bezafibrate induced increase in mitochondrial electron transport chain complex IV activity in human astrocytoma cells: Implications for mitochondrial cytopathies and neurodegenerative diseases
    Nicola Ioannou
    Department of Molecular Neuroscience, UCL Institute of Neurology, Queen Square, London, UK
    Biofactors 36:468-73. 2010
  6. ncbi Tetrahydrobiopterin availability in Parkinson's and Alzheimer's disease; potential pathogenic mechanisms
    Richard H Foxton
    Department of Molecular Neuroscience, Institute of Neurology, Queen Square, London, WC1N 3BG, UK
    Neurochem Res 32:751-6. 2007
  7. ncbi Neurodegeneration or neuroprotection: the pivotal role of astrocytes
    Simon J R Heales
    Division of Neurochemistry, Institute of Neurology, University College London, Queen Square, London, United Kingdom
    Neurochem Res 29:513-9. 2004
  8. ncbi A new perspective on the treatment of aromatic L-amino acid decarboxylase deficiency
    George F G Allen
    Department of Molecular Neuroscience, UCL Institute of Neurology, Queen Square House, Queen Square, London WC1N 3BG, UK
    Mol Genet Metab 97:6-14. 2009
  9. ncbi Phenotypic variability of mitochondrial disease caused by a nuclear mutation in complex II
    Alistair T Pagnamenta
    Biochemistry, Endocrinology and Metabolism Unit, Institute of Child Health, University College London, UK
    Mol Genet Metab 89:214-21. 2006

Collaborators

Detail Information

Publications9

  1. ncbi Some observations upon biochemical causes of ataxia and a new disease entity ubiquinone, CoQ10 deficiency
    John M Land
    Neurometabolic Unit Box 105, National Hospital for Neurology and Neurosurgery, Queen Square, London, WC1N 3BG, UK
    Neurochem Res 32:837-43. 2007
    ..Though rare, it is becoming increasingly recognised and patients are benefiting from the same scholarly approach to its investigation as was afforded Refsums' disease and Friedreich's ataxia...
  2. ncbi The effect of HMG-CoA reductase inhibitors on coenzyme Q10: possible biochemical/clinical implications
    Iain P Hargreaves
    Neurometabolic Unit, National Hospital for Neurology and Neurosurgery, Queen Square, London WC1N 3BG, UK
    Drug Saf 28:659-76. 2005
    ..This article reviews the biochemistry of CoQ(10), its role in cellular metabolism and the available evidence linking possible CoQ(10) deficiency to statin therapy...
  3. ncbi Determination of coenzyme Q10 status in blood mononuclear cells, skeletal muscle, and plasma by HPLC with di-propoxy-coenzyme Q10 as an internal standard
    Andrew J Duncan
    Division of Neurochemistry, Institute of Neurology, London, UK
    Clin Chem 51:2380-2. 2005
  4. ncbi Oxidative stress and mitochondrial dysfunction in neurodegeneration; cardiolipin a critical target?
    Simon Pope
    Neurometabolic Unit, National Hospital, UCLH Foundation Trust, UCL, Queen Square, London, WC1N 3BG, UK
    Biochim Biophys Acta 1777:794-9. 2008
    ....
  5. ncbi Bezafibrate induced increase in mitochondrial electron transport chain complex IV activity in human astrocytoma cells: Implications for mitochondrial cytopathies and neurodegenerative diseases
    Nicola Ioannou
    Department of Molecular Neuroscience, UCL Institute of Neurology, Queen Square, London, UK
    Biofactors 36:468-73. 2010
    ....
  6. ncbi Tetrahydrobiopterin availability in Parkinson's and Alzheimer's disease; potential pathogenic mechanisms
    Richard H Foxton
    Department of Molecular Neuroscience, Institute of Neurology, Queen Square, London, WC1N 3BG, UK
    Neurochem Res 32:751-6. 2007
    ..Such a cascade of events is hypothesized, in this article, to occur in neurodegenerative conditions such as Parkinson's and Alzheimer's disease...
  7. ncbi Neurodegeneration or neuroprotection: the pivotal role of astrocytes
    Simon J R Heales
    Division of Neurochemistry, Institute of Neurology, University College London, Queen Square, London, United Kingdom
    Neurochem Res 29:513-9. 2004
    ..In addition, depletion with time of the nitric oxide synthase cofactor, tetrahydrobiopterin, may result in the astrocytic generation of more potent oxidizing species, which could contribute to the neurodegenerative process...
  8. ncbi A new perspective on the treatment of aromatic L-amino acid decarboxylase deficiency
    George F G Allen
    Department of Molecular Neuroscience, UCL Institute of Neurology, Queen Square House, Queen Square, London WC1N 3BG, UK
    Mol Genet Metab 97:6-14. 2009
    ..Consequently gene therapy for AADC deficiency could be a realistic aim however an animal model of AADC deficiency is important for further progression...
  9. ncbi Phenotypic variability of mitochondrial disease caused by a nuclear mutation in complex II
    Alistair T Pagnamenta
    Biochemistry, Endocrinology and Metabolism Unit, Institute of Child Health, University College London, UK
    Mol Genet Metab 89:214-21. 2006
    ..Comparable activities and stability of mitochondrial respiratory chain enzymes were demonstrated in both patients, so other reasons for the phenotypic variability are considered...