Gary Gibson

Summary

Affiliation: Cornell University
Country: USA

Publications

  1. ncbi request reprint Mitochondrial function in fibroblasts with aging in culture and/or Alzheimer's disease
    Hsueh Meei Huang
    Weill Medical College, Cornell University, Burke Medical Research Institute, 785 Mamaroneck Avenue, White Plains, NY 10605, USA
    Neurobiol Aging 26:839-48. 2005
  2. pmc Abnormal thiamine-dependent processes in Alzheimer's Disease. Lessons from diabetes
    Gary E Gibson
    Department of Neurology and Neuroscience, Weill Cornell Medical College, Burke Medical Research Institute, 785 Mamaroneck Avenue, White Plains, NY 10605, USA
    Mol Cell Neurosci 55:17-25. 2013
  3. pmc Deficits in the mitochondrial enzyme α-ketoglutarate dehydrogenase lead to Alzheimer's disease-like calcium dysregulation
    Gary E Gibson
    Department of Neurology and Neuroscience, Weill Cornell Medical College, Burke Medical Research Institute, White Plains, NY 10605, USA
    Neurobiol Aging 33:1121.e13-24. 2012
  4. ncbi request reprint Interactions of oxidative stress with thiamine homeostasis promote neurodegeneration
    Gary E Gibson
    Burke Medical Research Institute, Weil Medical College, Cornell University, 785 Mamaroneck Avenue, White Plains, NY 10605, USA
    Neurochem Int 40:493-504. 2002
  5. ncbi request reprint Oxidative stress in Alzheimer's disease
    Gary E Gibson
    Weill Medical College of Cornell University, Burke Medical Research Institute, 785 Mamaroneck Avenue, White Plains, NY 10605, USA
    Neurobiol Aging 26:575-8. 2005
  6. ncbi request reprint Oxidative processes in the brain and non-neuronal tissues as biomarkers of Alzheimer's disease
    Gary E Gibson
    Weill Medical College of Cornell University at Burke Medical Research Institute, 785 Mamaroneck Avenue, White Plains, NY 10605, USA
    Front Biosci 7:d1007-15. 2002
  7. ncbi request reprint Oxidative stress increases internal calcium stores and reduces a key mitochondrial enzyme
    Gary E Gibson
    Cornell University Medical College at Burke Medical Research Institute, 785 Mamaroneck Avenue, White Plains, NY 10605, USA
    Biochim Biophys Acta 1586:177-89. 2002
  8. ncbi request reprint Interactions of oxidative stress with cellular calcium dynamics and glucose metabolism in Alzheimer's disease
    Gary E Gibson
    Weill Medical College of Cornell University, Burke Medical Research Institute, White Plains, NY 10605, USA
    Free Radic Biol Med 32:1061-70. 2002
  9. ncbi request reprint Selective response of various brain cell types during neurodegeneration induced by mild impairment of oxidative metabolism
    Zun Ji Ke
    Department of Neurology and Neuroscience, Weill Medical College of Cornell University at Burke Medical Research Institute, 785 Mamaroneck Avenue, White Plains, NY 10605, USA
    Neurochem Int 45:361-9. 2004
  10. ncbi request reprint The alpha-ketoglutarate-dehydrogenase complex: a mediator between mitochondria and oxidative stress in neurodegeneration
    Gary E Gibson
    Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York, NY, USA
    Mol Neurobiol 31:43-63. 2005

Research Grants

Collaborators

Detail Information

Publications62

  1. ncbi request reprint Mitochondrial function in fibroblasts with aging in culture and/or Alzheimer's disease
    Hsueh Meei Huang
    Weill Medical College, Cornell University, Burke Medical Research Institute, 785 Mamaroneck Avenue, White Plains, NY 10605, USA
    Neurobiol Aging 26:839-48. 2005
    ..This new, sensitive and quantitative estimate of relative MMP indicates that under non-stressed conditions relative MMP change with aging in culture, but relative MMP do not differ between controls and AD subjects...
  2. pmc Abnormal thiamine-dependent processes in Alzheimer's Disease. Lessons from diabetes
    Gary E Gibson
    Department of Neurology and Neuroscience, Weill Cornell Medical College, Burke Medical Research Institute, 785 Mamaroneck Avenue, White Plains, NY 10605, USA
    Mol Cell Neurosci 55:17-25. 2013
    ..This article is part of a Special Issue entitled 'Mitochondrial function and dysfunction in neurodegeneration'...
  3. pmc Deficits in the mitochondrial enzyme α-ketoglutarate dehydrogenase lead to Alzheimer's disease-like calcium dysregulation
    Gary E Gibson
    Department of Neurology and Neuroscience, Weill Cornell Medical College, Burke Medical Research Institute, White Plains, NY 10605, USA
    Neurobiol Aging 33:1121.e13-24. 2012
    ..The results suggest that the mitochondrial abnormalities in AD can be upstream of those in calcium...
  4. ncbi request reprint Interactions of oxidative stress with thiamine homeostasis promote neurodegeneration
    Gary E Gibson
    Burke Medical Research Institute, Weil Medical College, Cornell University, 785 Mamaroneck Avenue, White Plains, NY 10605, USA
    Neurochem Int 40:493-504. 2002
    ..The data indicate that the interactions of thiamine-dependent processes with oxidative stress are critical in neurodegenerative processes...
  5. ncbi request reprint Oxidative stress in Alzheimer's disease
    Gary E Gibson
    Weill Medical College of Cornell University, Burke Medical Research Institute, 785 Mamaroneck Avenue, White Plains, NY 10605, USA
    Neurobiol Aging 26:575-8. 2005
  6. ncbi request reprint Oxidative processes in the brain and non-neuronal tissues as biomarkers of Alzheimer's disease
    Gary E Gibson
    Weill Medical College of Cornell University at Burke Medical Research Institute, 785 Mamaroneck Avenue, White Plains, NY 10605, USA
    Front Biosci 7:d1007-15. 2002
    ..This review focuses on the considerable recent progress in the quest for markers of metabolism/oxidative stress in peripheral tissues from AD patients, and on experiments to test their pathophysiological importance...
  7. ncbi request reprint Oxidative stress increases internal calcium stores and reduces a key mitochondrial enzyme
    Gary E Gibson
    Cornell University Medical College at Burke Medical Research Institute, 785 Mamaroneck Avenue, White Plains, NY 10605, USA
    Biochim Biophys Acta 1586:177-89. 2002
    ..The findings support the hypothesis that select abnormalities in oxidative processes are a critical part of a cascade that leads to the cellular abnormalities in cells from AD patients...
  8. ncbi request reprint Interactions of oxidative stress with cellular calcium dynamics and glucose metabolism in Alzheimer's disease
    Gary E Gibson
    Weill Medical College of Cornell University, Burke Medical Research Institute, White Plains, NY 10605, USA
    Free Radic Biol Med 32:1061-70. 2002
    ..Prevention and/or correction of these abnormalities are appropriate therapeutic targets...
  9. ncbi request reprint Selective response of various brain cell types during neurodegeneration induced by mild impairment of oxidative metabolism
    Zun Ji Ke
    Department of Neurology and Neuroscience, Weill Medical College of Cornell University at Burke Medical Research Institute, 785 Mamaroneck Avenue, White Plains, NY 10605, USA
    Neurochem Int 45:361-9. 2004
    ..Although at early stages the responses of non-neuronal cells may be neuroprotective, at late phases they lead to entry of peripheral inflammatory cells into the brain and promote neurodegeneration...
  10. ncbi request reprint The alpha-ketoglutarate-dehydrogenase complex: a mediator between mitochondria and oxidative stress in neurodegeneration
    Gary E Gibson
    Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York, NY, USA
    Mol Neurobiol 31:43-63. 2005
    ..Studies of proteins, cells, animal models, and humans suggest that treatments to diminish, or bypass, the reduction in KGDHC might be beneficial in age-related neurodegenerative disorders...
  11. ncbi request reprint Thiamine-dependent processes and treatment strategies in neurodegeneration
    Gary E Gibson
    Department of Neurology and Neurosciences, Weill Medical College of Cornell University, Burke Medical Research Institute, White Plains, New York 10605, USA
    Antioxid Redox Signal 9:1605-19. 2007
    ..Adding thiamine or more absorbable forms of thiamine to tested treatments for the abnormality in glucose metabolism in AD may increase their efficacy...
  12. pmc Oxidant-induced changes in mitochondria and calcium dynamics in the pathophysiology of Alzheimer's disease
    Gary E Gibson
    Department of Neurology and Neuroscience, Weill Medical College of Cornell University, Burke Medical Research Institute, White Plains, NY 10605, USA
    Ann N Y Acad Sci 1147:221-32. 2008
    ..The results suggest that the reversal of mitochondrial deficits and a reduction in oxidative stress will reduce clinical and pathological changes and benefit patients...
  13. ncbi request reprint Differential alterations in antioxidant capacity in cells from Alzheimer patients
    G E Gibson
    Department of Neurology and Neuroscience, Weill Medical College of Cornell University, at Burke Medical Research Institute, 785 Mamaroneck Avenue, White Plains, NY 10605, USA
    Biochim Biophys Acta 1502:319-29. 2000
    ..The results demonstrate that fibroblasts bearing this PS-1 mutation have altered means of handling oxidative stress and appear useful for determining the mechanism underlying the altered redox metabolism...
  14. ncbi request reprint Abnormalities in Alzheimer's disease fibroblasts bearing the APP670/671 mutation
    G E Gibson
    Cornell University Medical College at Burke Medical Research Institute, White Plains, NY 10605, USA
    Neurobiol Aging 18:573-80. 1997
    ....
  15. pmc A mitocentric view of Alzheimer's disease suggests multi-faceted treatments
    Gary E Gibson
    Weill Cornell Medical College Burke Medical Research Institute, White Plains, NY, USA
    J Alzheimers Dis 20:S591-607. 2010
    ..Abnormalities in GMO diminish the ability of the brain to adapt. Therapies targeting mitochondria may ameliorate abnormalities in plaques, tangles, calcium homeostasis, and cognition that comprise AD...
  16. pmc Cause and consequence: mitochondrial dysfunction initiates and propagates neuronal dysfunction, neuronal death and behavioral abnormalities in age-associated neurodegenerative diseases
    Gary E Gibson
    Department of Neurology and Neuroscience, Weill Cornell Medical College of Cornell University at Burke Medical Research Institute, 785 Mamaroneck Avenue, White Plains, NY 10605, USA
    Biochim Biophys Acta 1802:122-34. 2010
    ..Altogether, our results suggest that increasing KGDHC via inhibition of TGase or via a host of other strategies to be described would be effective therapeutic approaches in age-associated neurodegenerative diseases...
  17. ncbi request reprint Oxidative stress and a key metabolic enzyme in Alzheimer brains, cultured cells, and an animal model of chronic oxidative deficits
    G E Gibson
    Department of Neurology and Neuroscience, Weill Medical College of Cornell University at Burke Medical Research Institute, White Plains, New York 10605, USA
    Ann N Y Acad Sci 893:79-94. 1999
    ..The results suggest that KGDHC participates in a deleterious cascade of events related to oxidative stress that are critical in selective neuronal loss in neurodegenerative diseases...
  18. ncbi request reprint The alpha-ketoglutarate dehydrogenase complex in neurodegeneration
    G E Gibson
    Department of Neurology and Neuroscience, Weill Medical College of Cornell University, Burke Medical Research Institute, White Plains, NY 10605, USA
    Neurochem Int 36:97-112. 2000
    ..Further studies are needed to assess mechanisms underlying the sensitivity of KGDHC to oxidative stress and the relation of KGDHC deficiency to selective vulnerability in neurodegenerative diseases...
  19. ncbi request reprint Foreword
    Gary E Gibson
    Weill Medical College of Cornell University, Burke Medical Research Institute, 785 Mamaroneck Avenue, White Plains, NY 10605, USA
    Neurochem Res 32:533-4. 2007
  20. ncbi request reprint Deficits in a tricarboxylic acid cycle enzyme in brains from patients with Parkinson's disease
    G E Gibson
    Weill Medical College of Cornell University, Burke Medical Research Institute, 785 Mamaroneck Avenue, White Plains, NY 10605, USA
    Neurochem Int 43:129-35. 2003
    ..Reductions in the activity of this enzyme, if widespread in the brain, may predispose vulnerable regions to further damage...
  21. pmc Mitochondrial dihydrolipoyl succinyltransferase deficiency accelerates amyloid pathology and memory deficit in a transgenic mouse model of amyloid deposition
    Magali Dumont
    Department of Neurology and Neuroscience, Weill Cornell Medical College, New York, NY 10065, USA
    Free Radic Biol Med 47:1019-27. 2009
    ..Our data suggest that alpha-KGDHC may be involved in AD pathogenesis through increased mitochondrial oxidative stress...
  22. ncbi request reprint Vascular factors are critical in selective neuronal loss in an animal model of impaired oxidative metabolism
    N Y Calingasan
    Weill Medical College of Cornell University at Burke Medical Research Institute, White Plains, New York 10605, USA
    J Neuropathol Exp Neurol 59:207-17. 2000
    ..Thus, TD provides a useful model to help elucidate the role of ICAM-1 and eNOS in the selective neuronal death in diseases in which oxidative stress is implicated...
  23. ncbi request reprint Mitochondrial impairment in the cerebellum of the patients with progressive supranuclear palsy
    L C Park
    Department of Neurology and Neuroscience, Weill Medical College of Cornell University, 785 Mamaroneck Avenue, White Plains, NY 10605, USA
    J Neurosci Res 66:1028-34. 2001
    ....
  24. ncbi request reprint Inherent abnormalities in energy metabolism in Alzheimer disease. Interaction with cerebrovascular compromise
    J P Blass
    Dementia Research Service, Burke Medical Research Institute, Weill Medical College of Cornell University, White Plains, New York 10605, USA
    Ann N Y Acad Sci 903:204-21. 2000
    ....
  25. ncbi request reprint Cerebrometabolic aspects of delirium in relationship to dementia
    J P Blass
    Cornell University Medical College, Burke Medical Research Institute, White Plains, NY 10605, USA
    Dement Geriatr Cogn Disord 10:335-8. 1999
    ..The clinical, metabolic, and pharmacological similarities between delirium and dementia agree with the suggestion that delirium and dementia can both be thought of as forms of 'cerebral insufficiency'...
  26. ncbi request reprint Frontal lobe dysfunction in progressive supranuclear palsy: evidence for oxidative stress and mitochondrial impairment
    D S Albers
    Department of Neurology and Neuroscience, Cornell University Medical College, New York, NY 10021, USA
    J Neurochem 74:878-81. 2000
    ..Together, these results suggest that mitochondrial dysfunction and lipid peroxidation may underlie the frontal metabolic and functional deficits observed in PSP...
  27. pmc Influence of mitochondrial enzyme deficiency on adult neurogenesis in mouse models of neurodegenerative diseases
    N Y Calingasan
    Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York, NY 10065, USA
    Neuroscience 153:986-96. 2008
    ..Our findings support the view that mitochondrial dysfunction can influence the number of neural progenitor cells in the hippocampus of adult mice...
  28. ncbi request reprint Metabolic impairment elicits brain cell type-selective changes in oxidative stress and cell death in culture
    L C Park
    Department of Neurology and Neuroscience, Weill Medical College of Cornell University at Burke Medical Research Institute, White Plains, New York 10605, USA
    J Neurochem 74:114-24. 2000
    ..The results demonstrate that the selective cell changes during TD in vivo reflect inherent properties of the different brain cell types...
  29. pmc Responses of the mitochondrial alpha-ketoglutarate dehydrogenase complex to thiamine deficiency may contribute to regional selective vulnerability
    Q Shi
    Department of Neurology and Neuroscience, Weill Medical College of Cornell University at Burke Medical Research Institute, 785 Mamaroneck Ave, White Plains, NY 10605, USA
    Neurochem Int 50:921-31. 2007
    ....
  30. ncbi request reprint Assessment of membrane potentials of mitochondrial populations in living cells
    H Zhang
    Weill Medical College of Cornell University at Burke Medical Research Institute, White Plains, New York 10605, USA
    Anal Biochem 298:170-80. 2001
    ..9 mV) and N2a cells (-81 +/- 0.7 mV) were very different by this method. This approach bridges investigations of individual mitochondria to those that assess MMP by examining global fluorescence from cells...
  31. ncbi request reprint Dopaminergic cell death induced by MPP(+), oxidant and specific neurotoxicants shares the common molecular mechanism
    H S Chun
    Department of Neurology and Neuroscience, Weill Medical College of Cornell University at The W.M. Burke Medical Research Institute, New York, USA
    J Neurochem 76:1010-21. 2001
    ....
  32. ncbi request reprint Co-culture with astrocytes or microglia protects metabolically impaired neurons
    L C Park
    Department of Neurology and Neuroscience, Weill Medical College of Cornell University at Burke Medical Research Institute, 785 Mamaroneck Avenue, White Plains, NY 10605, USA
    Mech Ageing Dev 123:21-7. 2001
    ..Thus, neuronal-glial interactions are critical for maintaining neuronal homeostasis during chronic metabolic impairment...
  33. ncbi request reprint Effect of age on behavioral and enzymatic changes during thiamin deficiency
    G B Freeman
    Cornell University Medical College, Burke Rehabilitation Center, White Plains, NY 10605
    Neurobiol Aging 8:429-34. 1987
    ..Thus, the current mouse model is an attractive one to study the interaction of thiamin deficiency with aging...
  34. ncbi request reprint Enzyme-catalyzed side reactions with molecular oxygen may contribute to cell signaling and neurodegenerative diseases
    Victoria I Bunik
    School of Bioengineering and Bioinformatics, and Belozersky Institute of Physico Chemical Biology, Moscow State University, Moscow 119992, Russia
    Neurochem Res 32:871-91. 2007
    ....
  35. pmc Changes in inflammatory processes associated with selective vulnerability following mild impairment of oxidative metabolism
    Saravanan S Karuppagounder
    Department of Neurology and Neuroscience, Weill Medical College of Cornell University, Burke Medical Research Institute, 785 Mamaroneck Avenue, White Plains, NY 10605, USA
    Neurobiol Dis 26:353-62. 2007
    ..The results demonstrate that TD induces quantitative, distinct inflammatory responses and oxidative stress in vulnerable and non-vulnerable regions that may underlie selective vulnerability...
  36. pmc Oxidative stress and transcriptional regulation in Alzheimer disease
    Qingli Shi
    Department of Neurology and Neuroscience, Weill Medical College of Cornell University, Burke Medical Research Institute, White Plains, NY 10605, USA
    Alzheimer Dis Assoc Disord 21:276-91. 2007
    ..Finally, potential therapeutic strategies based on the updated understandings of redox state-dependent gene regulation in AD are proposed to overcome the lack of efficacy of antioxidant therapies...
  37. pmc Novel functions of the alpha-ketoglutarate dehydrogenase complex may mediate diverse oxidant-induced changes in mitochondrial enzymes associated with Alzheimer's disease
    Qingli Shi
    Department of Neurology and Neuroscience, Weill Medical College of Cornell University Burke Medical Research Institute, White Plains, New York 10605, USA
    Biochim Biophys Acta 1782:229-38. 2008
    ....
  38. ncbi request reprint Inhibition of the alpha-ketoglutarate dehydrogenase complex by the myeloperoxidase products, hypochlorous acid and mono-N-chloramine
    Thomas M Jeitner
    Department of Biochemistry, Medical College of Wisconsin, Milwaukee, Wisconsin, USA
    J Neurochem 92:302-10. 2005
    ..Thus, hypochlorous acid and chloramines have the potential to inactivate a major target in neurodegeneration...
  39. ncbi request reprint Reversal of thiamine deficiency-induced neurodegeneration
    Zun Ji Ke
    Department of Neurology and Neuroscience, Weill Medical College of Cornell University at Burke Medical Research Institute, White Plains, New York, USA
    J Neuropathol Exp Neurol 62:195-207. 2003
    ..endothelial cells, and microglia contemporaneously. This model provides a unique paradigm for elucidating the molecular mechanisms involved in neuronal commitment to neuronal death cascades and contributory microglial activity...
  40. pmc Translocation of amyloid precursor protein C-terminal fragment(s) to the nucleus precedes neuronal death due to thiamine deficiency-induced mild impairment of oxidative metabolism
    Saravanan S Karuppagounder
    Department of Neurology and Neuroscience, Weill Medical College of Cornell University, Burke Medical Research Institute, 785 Mamaroneck Avenue, White Plains, NY 10605, USA
    Neurochem Res 33:1365-72. 2008
    ..TD did not alter CTF 15 or CTF 12 levels in cortex. These findings demonstrate that changes in APP metabolism occur in early stages of TD, and they may play an important role in TD-induced selective neuronal loss...
  41. ncbi request reprint Correlations of disability and biologic alterations in Alzheimer brain and test of significance by a therapeutic trial in humans
    John P Blass
    Weil Medical College of Cornell University, Burke Medical Research Institute, 785 Mamaroneck Ave White Plains, NY 10605, USA
    J Alzheimers Dis 9:207-18. 2006
    ..The clinical value of treatments of the cerebrometabolic deficiency in AD warrants further investigation...
  42. ncbi request reprint Modification of endoplasmic reticulum Ca2+ stores by select oxidants produces changes reminiscent of those in cells from patients with Alzheimer disease
    Hsueh Meei Huang
    Weill Medical College of Cornell University at Burke Medical Research Institute, 785 Mamaroneck Avenue, White Plains, NY 10605, USA
    Free Radic Biol Med 39:979-89. 2005
    ..Thus, these results are consistent with the hypothesis that abnormalities in selective cellular ROS cause AD-related changes in intracellular calcium regulation...
  43. ncbi request reprint Inhibition of alpha-ketoglutarate dehydrogenase complex promotes cytochrome c release from mitochondria, caspase-3 activation, and necrotic cell death
    Hsueh Meei Huang
    Weill Medical College of Cornell University, Burke Medical Research Institute, White Plains, New York 10605, USA
    J Neurosci Res 74:309-17. 2003
    ..Thus, impairment of this key mitochondrial enzyme in PC12 cells may lead to cytochrome c release and caspase-3 activation by partial opening of the MPTP before the loss of mitochondrial membrane potentials...
  44. ncbi request reprint Mice deficient in dihydrolipoamide dehydrogenase show increased vulnerability to MPTP, malonate and 3-nitropropionic acid neurotoxicity
    Peter Klivenyi
    Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York Presbyterian Hospital, New York 10021, USA
    J Neurochem 88:1352-60. 2004
    ..KGDHC activity was also found to be reduced in putamen from patients with HD. These findings provide further evidence that mitochondrial defects may contribute to the pathogenesis of neurodegenerative diseases...
  45. ncbi request reprint Inhibition of the alpha-ketoglutarate dehydrogenase complex alters mitochondrial function and cellular calcium regulation
    Hsueh Meei Huang
    Dementia Research Service, Weill Medical College of Cornell University, Burke Medical Res Institute, 785 Mamaroneck Avenue, White Plains, NY 10605, USA
    Biochim Biophys Acta 1637:119-26. 2003
    ..Reductions in this key mitochondrial enzyme will likely make the cells more vulnerable to metabolic insults that promote cell death...
  46. ncbi request reprint The role of the metabolic lesion in Alzheimer's disease
    John P Blass
    Weill Cornell Medical College at Burke Medical Research Institute, 785 Mamaroneck Ave, White Plains, NY 10605, USA
    J Alzheimers Dis 4:225-32. 2002
    ..However, those other abnormalities including amyloidosis can occur in people whose mentation is still clinically unimpaired. In contrast, once significant decrease in the rate of brain metabolism occurs, mentation becomes defective...
  47. ncbi request reprint Mitochondrial enzymes and endoplasmic reticulum calcium stores as targets of oxidative stress in neurodegenerative diseases
    Gary E Gibson
    Burke Medical Research Institute, Weill Medical College of Cornell University, 785 Mamaroneck Avenue, White Plains, New York 10605, USA
    J Bioenerg Biomembr 36:335-40. 2004
    ..The results suggest that KGDHC and BRCS provide targets by which oxidative stress may induce neurodegeneration and a useful tool for selecting antioxidants for reversing age-related neurodegeneration...
  48. ncbi request reprint alpha-keto-beta-methyl-n-valeric acid diminishes reactive oxygen species and alters endoplasmic reticulum Ca(2+) stores
    Hsueh Meei Huang
    Weill Medical College of Cornell University, Burke Medical Research Institute, White Plains, NY 10605, USA
    Free Radic Biol Med 37:1779-89. 2004
    ..The same H(2)O(2)-induced ROS that reacts with KMV may also underlie the changes in BRCS related to AD. Thus, KMV ameliorates the effects of ROS on calcium homeostasis related to oxidative stress and to AD...
  49. ncbi request reprint Mitochondrial abnormalities in Alzheimer brain: mechanistic implications
    Parvesh Bubber
    Weill Medical College of Cornell University at Burke Medical Research Institute, White Plains, NY 10605, USA
    Ann Neurol 57:695-703. 2005
    ..01), suggesting a coordinated mitochondrial alteration. The highest correlation was with pyruvate dehydrogenase complex (r = 0.77, r2= 0.59). Measures to improve TCA cycle metabolism might benefit AD patients...
  50. ncbi request reprint CD40-CD40L interactions promote neuronal death in a model of neurodegeneration due to mild impairment of oxidative metabolism
    Zun Ji Ke
    Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York, NY, USA
    Neurochem Int 47:204-15. 2005
    ..The results indicate that CD40-CD40L interactions promote neuronal death in early stages of TD, but that at later phases the protective effects of the diminished CD40 or CD40L are over-ridden by other mechanisms...
  51. ncbi request reprint CD40L deletion delays neuronal death in a model of neurodegeneration due to mild impairment of oxidative metabolism
    Zun Ji Ke
    Institute for Nutritional Sciences, SIBS, CAS, 294 Taiyuan Road, Shanghai 200031, PR China
    J Neuroimmunol 164:85-92. 2005
    ..The current results suggest that CD40L-mediated immune and inflammatory responses have a role in TD-induced neuronal death...
  52. ncbi request reprint Inhibitors of the alpha-ketoglutarate dehydrogenase complex alter [1-13C]glucose and [U-13C]glutamate metabolism in cerebellar granule neurons
    Sónia Sá Santos
    Instituto de Biologia Experimental e Tecnológica Instituto de Tecnologia Quimica e Biológica IBET ITQB, Oeiras, Portugal
    J Neurosci Res 83:450-8. 2006
    ..The results suggest the potential of succinyl phosphonate esters for modeling the biochemical and pathophysiological consequences of reduced KGDHC activity in brain diseases...
  53. ncbi request reprint Phospholipid mass is increased in fibroblasts bearing the Swedish amyloid precursor mutation
    Eric J Murphy
    Department of Pharmacology, Physiology, and Therapeutics and Department of Chemistry, School of Medicine and Health Sciences, University of North Dakota, 501 N Columbia Road, Room 3700, Grand Forks, ND 58202 9037, USA
    Brain Res Bull 69:79-85. 2006
    ....
  54. ncbi request reprint Peripheral inflammatory mechanisms modulate microglial activation in response to mild impairment of oxidative metabolism
    Zun Ji Ke
    Institution for Nutritional Sciences, SIBS, CAS, 294 Taiyuan Rd, Shanghai, China
    Neurochem Int 49:548-56. 2006
    ....
  55. ncbi request reprint Cisplatin-induced toxicity is associated with platinum deposition in mouse kidney mitochondria in vivo and with selective inactivation of the alpha-ketoglutarate dehydrogenase complex in LLC-PK1 cells
    Lei Zhang
    Department of Cell Biology, Biomedical Research Center, Room 264, 975 N E 10th Street, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma 73104, USA
    Biochemistry 45:8959-71. 2006
    ....
  56. ncbi request reprint Mitochondrial enzymes in schizophrenia
    Parvesh Bubber
    Department of Neurology and Neuroscience, Weill Medical College of Cornell University at Burke Medical Research Institute, White Plains, NY, 10605, USA
    J Mol Neurosci 24:315-21. 2004
    ..However, in schizophrenia, unlike a number of neurodegenerative diseases, reductions in the activities of the key mitochondrial enzymes KGDHC and PDHC are not frequent...
  57. ncbi request reprint Mitochondrial aconitase is a transglutaminase 2 substrate: transglutamination is a probable mechanism contributing to high-molecular-weight aggregates of aconitase and loss of aconitase activity in Huntington disease brain
    Soo Youl Kim
    Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York, NY 10021, USA
    Neurochem Res 30:1245-55. 2005
    ..The present findings suggest that an increase of transglutaminase activity in HD caudate may contribute to mitochondrial dysfunction by incorporating aconitase into inactive polymers...
  58. ncbi request reprint Reduction in the E2k subunit of the alpha-ketoglutarate dehydrogenase complex has effects independent of complex activity
    Qingli Shi
    Department of Neurology and Neuroscience, Weill Medical College of Cornell University at Burke Medical Research Institute, White Plains, New York 10605, USA
    J Biol Chem 280:10888-96. 2005
    ..These results suggest that in addition to its essential role in metabolism, the E2k component of KGDHC may have other novel roles...
  59. ncbi request reprint Tricarboxylic acid cycle enzymes following thiamine deficiency
    Parvesh Bubber
    Department of Neurology and Neuroscience, Burke Medical Research Institute, Weill Medical College, Cornell University, 785 Mamaroneck Avenue, White Plains, NY 10605, USA
    Neurochem Int 45:1021-8. 2004
    ..The diminished activities of multiple TCA cycle enzymes may be important in our understanding of how metabolic lesions alter brain function in neurodegenerative disorders...
  60. ncbi request reprint Mitochondrial heterogeneity within and between different cell types
    Hsueh Meei Huang
    Dementia Research Service, Department of Neurology and Neuroscience, Weill Medical College of Cornell University at Burke Medical Research Institute, 785 Mamaroneck Avenue, White Plains, New York 10605, USA
    Neurochem Res 29:651-8. 2004
    ..Although biological implications of heterogeneity of MMP are not clear, this approach provides a tool to address this question...
  61. pmc Transglutaminase activity is present in highly purified nonsynaptosomal mouse brain and liver mitochondria
    Boris F Krasnikov
    Department of Neurology and Neurosciences, and Medicine, Weill Medical College of Cornell University, New York City, New York 10021, USA
    Biochemistry 44:7830-43. 2005
    ..This activity may play a role in regulation of mitochondrial function both in normal physiology and in disease. Its nature and regulation deserve further study...
  62. ncbi request reprint Phosphonate analogues of alpha-ketoglutarate inhibit the activity of the alpha-ketoglutarate dehydrogenase complex isolated from brain and in cultured cells
    Victoria I Bunik
    School of Bioinformatics and Bioengineering and Belozersky Institute of Physico Chemical Biology, Moscow State University, Moscow 119992, Russian Federation
    Biochemistry 44:10552-61. 2005
    ....

Research Grants22

  1. SIGNAL TRANSDUCTION SYSTEMS IN ALZHEIMERS DISEASE
    Gary Gibson; Fiscal Year: 2003
    ..abstract_text> ..
  2. Mitochondiral enzymes/oxidative stress in Alzheimer's
    Gary Gibson; Fiscal Year: 2004
    ..These models will also provide systems to test the efficacy of approaches to limit or reverse the changes in mitochondria. ..
  3. AGE/NUTRITION/GENES IN MODELS OF PSYCHIATRIC DISORDERS
    Gary Gibson; Fiscal Year: 2007
    ..An understanding of these mechanisms will likely suggest new ways to overcome the consequences of the mild, chronic impairment of oxidative metabolism that accompanies numerous age-related neurodegenerative disorders. ..