James P Bennett

Summary

Affiliation: Virginia Commonwealth University
Country: USA

Publications

  1. pmc RhTFAM treatment stimulates mitochondrial oxidative metabolism and improves memory in aged mice
    Ravindar R Thomas
    Parkinson s Disease Center, Virginia Commonwealth University, Richmond, VA 23298, USA
    Aging (Albany NY) 4:620-35. 2012
  2. pmc ALS spinal neurons show varied and reduced mtDNA gene copy numbers and increased mtDNA gene deletions
    Paula M Keeney
    Department of Neurology, University of Virginia, Charlottesville, Virginia, USA
    Mol Neurodegener 5:21. 2010
  3. pmc Parkinson's disease brain mitochondria have impaired respirasome assembly, age-related increases in distribution of oxidative damage to mtDNA and no differences in heteroplasmic mtDNA mutation abundance
    Charles R Arthur
    Morris K Udall Parkinson s Disease Research Center of Excellence, University of Virginia School of Medicine, Charlottesville, VA 22908, USA
    Mol Neurodegener 4:37. 2009
  4. doi request reprint Nerve growth factor attenuates oxidant-induced β-amyloid neurotoxicity in sporadic Alzheimer's disease cybrids
    Isaac G Onyango
    Department of Neurology, University of Kansas Medical Center, Kansas City, Kansas, USA
    J Neurochem 114:1605-18. 2010
  5. pmc Mitochondrial gene therapy augments mitochondrial physiology in a Parkinson's disease cell model
    Paula M Keeney
    Morris K Udall Parkinson s Disease Research Center of Excellence, University of Virginia, Charlottesville, VA 22908, USA
    Hum Gene Ther 20:897-907. 2009
  6. pmc Recombinant human mitochondrial transcription factor A stimulates mitochondrial biogenesis and ATP synthesis, improves motor function after MPTP, reduces oxidative stress and increases survival after endotoxin
    Ravindar R Thomas
    Morris Udall Parkinson s Disease Research Center of Excellence, University of Virginia, Charlottesville, VA, United States
    Mitochondrion 11:108-18. 2011
  7. pmc Relationships among molecular genetic and respiratory properties of Parkinson's disease cybrid cells show similarities to Parkinson's brain tissues
    M Kathleen Borland
    Center for the Study of Neurodegenerative Diseases, University of Virginia, Charlottesville, Virginia, USA
    Biochim Biophys Acta 1792:68-74. 2009
  8. ncbi request reprint Altered intracellular signaling and reduced viability of Alzheimer's disease neuronal cybrids is reproduced by beta-amyloid peptide acting through receptor for advanced glycation end products (RAGE)
    Isaac G Onyango
    Center for the Study of Neurodegenerative Diseases, University of Virginia School of Medicine, Charlottesville, VA 22908, USA
    Mol Cell Neurosci 29:333-43. 2005
  9. pmc Recombinant mitochondrial transcription factor A with N-terminal mitochondrial transduction domain increases respiration and mitochondrial gene expression
    Shilpa Iyer
    Center for the Study of Neurodegenerative Diseases and The Morris K Udall Parkinson s Disease Research Center of Excellence, University of Virginia, PO Box 800394, Charlottesville, VA 22908, United States
    Mitochondrion 9:196-203. 2009
  10. pmc Mitochondrial quality, dynamics and functional capacity in Parkinson's disease cybrid cell lines selected for Lewy body expression
    Emily N Cronin-Furman
    Parkinson s and Movement Disorders Center, Virginia Commonwealth University, Richmond, VA 23298, USA
    Mol Neurodegener 8:6. 2013

Research Grants

  1. OXIDATIVE STRESS IN PARKINSON'S DISEASE
    James Bennett; Fiscal Year: 2000
  2. OXIDATIVE STRESS IN PARKINSON'S DISEASE
    James Bennett; Fiscal Year: 2001
  3. OXIDATIVE STRESS IN PARKINSON'S DISEASE
    James Bennett; Fiscal Year: 2001
  4. OXIDATIVE STRESS IN PARKINSON'S DISEASE
    James Bennett; Fiscal Year: 2002
  5. OXIDATIVE STRESS IN PARKINSON'S DISEASE
    James Bennett; Fiscal Year: 2002
  6. OXIDATIVE STRESS IN PARKINSON'S DISEASE
    James Bennett; Fiscal Year: 2003
  7. OXIDATIVE STRESS IN PARKINSON'S DISEASE
    James Bennett; Fiscal Year: 2004

Collaborators

Detail Information

Publications33

  1. pmc RhTFAM treatment stimulates mitochondrial oxidative metabolism and improves memory in aged mice
    Ravindar R Thomas
    Parkinson s Disease Center, Virginia Commonwealth University, Richmond, VA 23298, USA
    Aging (Albany NY) 4:620-35. 2012
    ....
  2. pmc ALS spinal neurons show varied and reduced mtDNA gene copy numbers and increased mtDNA gene deletions
    Paula M Keeney
    Department of Neurology, University of Virginia, Charlottesville, Virginia, USA
    Mol Neurodegener 5:21. 2010
    ..It is presently unknown whether mtDNA abnormalities are present in single human ALS neurons...
  3. pmc Parkinson's disease brain mitochondria have impaired respirasome assembly, age-related increases in distribution of oxidative damage to mtDNA and no differences in heteroplasmic mtDNA mutation abundance
    Charles R Arthur
    Morris K Udall Parkinson s Disease Research Center of Excellence, University of Virginia School of Medicine, Charlottesville, VA 22908, USA
    Mol Neurodegener 4:37. 2009
    ..abstract:..
  4. doi request reprint Nerve growth factor attenuates oxidant-induced β-amyloid neurotoxicity in sporadic Alzheimer's disease cybrids
    Isaac G Onyango
    Department of Neurology, University of Kansas Medical Center, Kansas City, Kansas, USA
    J Neurochem 114:1605-18. 2010
    ....
  5. pmc Mitochondrial gene therapy augments mitochondrial physiology in a Parkinson's disease cell model
    Paula M Keeney
    Morris K Udall Parkinson s Disease Research Center of Excellence, University of Virginia, Charlottesville, VA 22908, USA
    Hum Gene Ther 20:897-907. 2009
    ..It also is unclear whether single-donor gDNA for generating mtDNA would be a preferred therapeutic compared with the pooled gDNA used in this study...
  6. pmc Recombinant human mitochondrial transcription factor A stimulates mitochondrial biogenesis and ATP synthesis, improves motor function after MPTP, reduces oxidative stress and increases survival after endotoxin
    Ravindar R Thomas
    Morris Udall Parkinson s Disease Research Center of Excellence, University of Virginia, Charlottesville, VA, United States
    Mitochondrion 11:108-18. 2011
    ..rhTFAM treatment improved motor recovery rate after treatment with MPTP and dose-dependently improved survival in the lipopolysaccharide model of endotoxin sepsis...
  7. pmc Relationships among molecular genetic and respiratory properties of Parkinson's disease cybrid cells show similarities to Parkinson's brain tissues
    M Kathleen Borland
    Center for the Study of Neurodegenerative Diseases, University of Virginia, Charlottesville, Virginia, USA
    Biochim Biophys Acta 1792:68-74. 2009
    ..This will require characterization of the abnormalities and dynamics of mtDNA changes propagated through sPD cybrids over time...
  8. ncbi request reprint Altered intracellular signaling and reduced viability of Alzheimer's disease neuronal cybrids is reproduced by beta-amyloid peptide acting through receptor for advanced glycation end products (RAGE)
    Isaac G Onyango
    Center for the Study of Neurodegenerative Diseases, University of Virginia School of Medicine, Charlottesville, VA 22908, USA
    Mol Cell Neurosci 29:333-43. 2005
    ..This SAD phenotype is produced by endogenously generated Abeta and can be replicated by exogenous Abeta acting through RAGE...
  9. pmc Recombinant mitochondrial transcription factor A with N-terminal mitochondrial transduction domain increases respiration and mitochondrial gene expression
    Shilpa Iyer
    Center for the Study of Neurodegenerative Diseases and The Morris K Udall Parkinson s Disease Research Center of Excellence, University of Virginia, PO Box 800394, Charlottesville, VA 22908, United States
    Mitochondrion 9:196-203. 2009
    ..MTD-TFAM increases mitochondrial bioenergetics and holds promise for treatment of mitochondrial diseases involving deficiencies of energy production...
  10. pmc Mitochondrial quality, dynamics and functional capacity in Parkinson's disease cybrid cell lines selected for Lewy body expression
    Emily N Cronin-Furman
    Parkinson s and Movement Disorders Center, Virginia Commonwealth University, Richmond, VA 23298, USA
    Mol Neurodegener 8:6. 2013
    ..We studied mitochondrial morphology, bioenergetics and biogenesis signaling by creating stable sub-clones of three PD cybrid cell lines derived from cells expressing CLB...
  11. ncbi request reprint Brain-derived growth factor and glial cell line-derived growth factor use distinct intracellular signaling pathways to protect PD cybrids from H2O2-induced neuronal death
    Isaac G Onyango
    Department of Neuroscience, University of Virginia School of Medicine, PO Box 801392, Charlottesville, VA 22908, USA
    Neurobiol Dis 20:141-54. 2005
    ....
  12. pmc Cybrid models of Parkinson's disease show variable mitochondrial biogenesis and genotype-respiration relationships
    Paula M Keeney
    Morris K Udall Parkinson s Research Center of Excellence, University of Virginia, PO Box 800394, Charlottesville, VA 22908, USA
    Exp Neurol 220:374-82. 2009
    ..Cybrids remain a valuable model for some aspects of sPD but their heterogeneity mitigates against a simple designation of sPD phenotype in this cell model...
  13. pmc The cybrid model of sporadic Parkinson's disease
    Patricia A Trimmer
    Morris K Udall Parkinson s Disease Research Center of Excellence, Department of Neurology, University of Virginia, Charlottesville, 22908, USA
    Exp Neurol 218:320-5. 2009
    ..sPD cybrid models can be improved by the use of non-tumor human stem cell-derived neural precursor cells and by an introduction of postmortem brain mtDNA to test its causality directly...
  14. ncbi request reprint Impaired complex-I mitochondrial biogenesis in Parkinson disease frontal cortex
    Ravindar R Thomas
    Parkinson s Disease Research Center, Virginia Commonwealth University, Richmond, VA 23298, USA
    J Parkinsons Dis 2:67-76. 2012
    ..Stimulation of mitobiogenesis in PD may inhibit rostral disease progression and appearance of secondary symptoms referable to frontal cortex...
  15. ncbi request reprint Parkinson's disease transgenic mitochondrial cybrids generate Lewy inclusion bodies
    Patricia A Trimmer
    Center for the Study of Neurodegenerative Diseases and Department of Neurology, University of Virginia, School of Medicine, Charlottesville, Virginia 22908, USA
    J Neurochem 88:800-12. 2004
    ..Future studies of these cybrids will enable us to better understand how Lewy bodies form and what role they play in the pathogenesis of PD...
  16. ncbi request reprint Cyclical mitochondrial deltapsiM fluctuations linked to electron transport, F0F1 ATP-synthase and mitochondrial Na+/Ca+2 exchange are reduced in Alzheimer's disease cybrids
    Christine Thiffault
    Department of Neurology, Center for the Study of Neurodegenerative Diseases, University of Virginia, PO Box 800394, Charlottesville, VA 22908, USA
    Mitochondrion 5:109-19. 2005
    ..AD cybrid mitochondria showed reduced flickering. Flickering seems to represent coupling of deltapsiM to F0F1 ATP-synthase; reduction of flickering in AD cybrids suggests dysfunction of this coupling...
  17. ncbi request reprint Interactions among nitric oxide and Bcl-family proteins after MPP+ exposure of SH-SY5Y neural cells II: exogenous NO replicates MPP+ actions
    Jameel Dennis
    Neuroscience Graduate Program, University of Virginia School of Medicine, Charlottesville, Virginia 22908, USA
    J Neurosci Res 72:89-97. 2003
    ..Our results show that exogenous NO mimics actions of MPP(+) on SH-SY5Y neuroblastoma cells and supports the mediation of MPP(+) neurotoxicity by NO generated intracellularly in mitochondria...
  18. ncbi request reprint Neurotoxic nitric oxide rapidly depolarizes and permeabilizes mitochondria by dynamically opening the mitochondrial transition pore
    Dean D Kindler
    Center for the Study of Neurodegenerative Diseases and Department of Neurology, University of Virginia, Charlottesville, VA 22908, USA
    Mol Cell Neurosci 23:559-73. 2003
    ..Our findings show rapid-onset, dynamic regulation of Deltapsi M by NO, implying that neuroprotective therapies for brain ischemia target cell death processes downstream of effects of NO on mitochondria...
  19. ncbi request reprint Endogenous oxidative stress in sporadic Alzheimer's disease neuronal cybrids reduces viability by increasing apoptosis through pro-death signaling pathways and is mimicked by oxidant exposure of control cybrids
    Isaac G Onyango
    Center for the Study of Neurodegenerative Diseases, University of Virginia School of Medicine, Charlottesville, VA 22908, USA
    Neurobiol Dis 19:312-22. 2005
    ..Exposure of CTL cybrids to H2O2 decreased viability and activated in a NAC-sensitive manner, the same intracellular signaling pathways active under basal conditions in SAD cybrids...
  20. ncbi request reprint Dependence on electron transport chain function and intracellular signaling of genomic responses in SH-SY5Y cells to the mitochondrial neurotoxin MPP(+)
    Louis B Brill
    Center for the Study of Neurodegenerative Diseases and Medical Scientist Training Program, University of Virginia, Charlottesville, VA 22908, USA
    Exp Neurol 181:25-38. 2003
    ..Genes suppressed by UO 126 or LY 294002 during MPP(+) exposure may mediate cell survival; those expressed in the presence of UO 126 or LY 294002 may mediate cell death in this in vitro model of Parkinson's disease...
  21. ncbi request reprint Activation of p38 and N-acetylcysteine-sensitive c-Jun NH2-terminal kinase signaling cascades is required for induction of apoptosis in Parkinson's disease cybrids
    Isaac G Onyango
    Center for the Study of Neurodegenerative Diseases, University of Virginia School of Medicine, Charlottesville, Virginia 22908, USA
    Mol Cell Neurosci 28:452-61. 2005
    ..PD mitochondrial genes expressed in cybrids stimulate pro-apoptotic cell signaling and biochemistry through oxidative stress. These results support development of antioxidative therapeutics for PD...
  22. ncbi request reprint Parkinson's disease brain mitochondrial complex I has oxidatively damaged subunits and is functionally impaired and misassembled
    Paula M Keeney
    Center for the Study of Neurodegenerative Diseases, University of Virginia, Charlottesville, Virginia 22908, USA
    J Neurosci 26:5256-64. 2006
    ..This complex I auto-oxidation may derive from abnormalities in mitochondrial or nuclear encoded subunits, complex I assembly factors, rotenone-like complex I toxins, or some combination...
  23. pmc Mitochondrial gene therapy improves respiration, biogenesis, and transcription in G11778A Leber's hereditary optic neuropathy and T8993G Leigh's syndrome cells
    Shilpa Iyer
    Center for the Study of Biological Complexity, Life Sciences, Virginia Commonwealth University, Richmond, VA 23284 3020, USA
    Hum Gene Ther 23:647-57. 2012
    ..These results represent the development of a therapeutic approach for LHON and LS patients in the near future...
  24. doi request reprint The dying of the light: mitochondrial failure in Alzheimer's disease
    Kisha J Young-Collier
    Neuroscience Graduate Program and Medical Scientist Training Program, University of Virginia School of Medicine, Charlottesville, VA, USA
    J Alzheimers Dis 28:771-81. 2012
    ..Downregulation of antioxidant proteins further threatens neuronal function. Altering progression of AD appears to require both correction of impaired mitobiogenesis and restoration of antioxidant protection...
  25. pmc Chronic, low-dose rotenone reproduces Lewy neurites found in early stages of Parkinson's disease, reduces mitochondrial movement and slowly kills differentiated SH-SY5Y neural cells
    M Kathleen Borland
    Center for the Study of Neurodegenerative Diseases and Morris K, Udall Parkinson s Disease Research Center of Excellence, University of Virginia, Charlottesville, Virginia, USA
    Mol Neurodegener 3:21. 2008
    ..The vast majority of Parkinson's disease occurs sporadically, and current models of sporadic Parkinson's disease (sPD) can utilize directly infused or systemic neurotoxins...
  26. ncbi request reprint The mitochondrial secret(ase) of Alzheimer's disease
    Kisha J Young
    Neuroscience Graduate Program and Medical Scientist Training Program, University of Virginia School of Medicine, Charlottesville, VA, USA
    J Alzheimers Dis 20:S381-400. 2010
    ....
  27. ncbi request reprint Mitochondrial abnormalities in cybrid cell models of sporadic Alzheimer's disease worsen with passage in culture
    Patricia A Trimmer
    Center for the Study of Neurodegenerative Diseases, University of Virginia School of Medicine, Charlottesville, VA 22908, USA
    Neurobiol Dis 15:29-39. 2004
    ..Metabolically deleterious SAD mitochondrial genes, like those in yeast, may have a replicative advantage over nondeleterious mitochondrial genes that assume dominance in CTL cybrids...
  28. ncbi request reprint Interactions among nitric oxide and Bcl-family proteins after MPP+ exposure of SH-SY5Y neural cells I: MPP+ increases mitochondrial NO and Bax protein
    Jameel Dennis
    Neuroscience Graduate Program, University of Virginia School of Medicine, Charlottesville, Virginia 00908, USA
    J Neurosci Res 72:76-88. 2003
    ....
  29. ncbi request reprint Postmenopausal estrogen use affects risk for Parkinson disease
    Lillian J Currie
    Department of Neurology, School of Medicine, University of Virginia Health System, Charlottesville, VA 22908, USA
    Arch Neurol 61:886-8. 2004
    ....
  30. ncbi request reprint Development of mitochondrial gene replacement therapy
    Shaharyar M Khan
    Center for the Study of Neurodegenerative Diseases, University of Virginia, Charlottesville, Virginia, USA
    J Bioenerg Biomembr 36:387-93. 2004
    ..Protofection also delivers mtDNA in vivo, opening the way to rational development of mitochondrial gene replacement therapy of mtDNA-based diseases...
  31. ncbi request reprint Mitochondrial DNA copy numbers in pyramidal neurons are decreased and mitochondrial biogenesis transcriptome signaling is disrupted in Alzheimer's disease hippocampi
    Ann C Rice
    Parkinson s Disease Center, Virginia Commonwealth University, Richmond, VA, USA Department of Neurology, Virginia Commonwealth University, Richmond, VA, USA
    J Alzheimers Dis 40:319-30. 2014
    ..Mitochondrial biogenesis pathway signaling relationships are disrupted in AD, but are mostly preserved in CTL. Our findings implicate complex alterations of mitochondria-host cell relationships in AD. ..
  32. doi request reprint R+ pramipexole as a mitochondrially focused neuroprotectant: initial early phase studies in ALS
    Hua Wang
    Department of Neurology, University of Virginia School of Medicine, Charlottesville, Virginia, USA
    Amyotroph Lateral Scler 9:50-8. 2008
    ..High doses of R+PPX were tolerated well and yielded neuroprotective plasma levels. These findings support longer-term testing of higher R+PPX doses as a potential disease-altering therapy for SALS...
  33. ncbi request reprint Stability of gene expression in postmortem brain revealed by cDNA gene array analysis
    Stacey A Trotter
    Center for the Study of Neurodegenerative Diseases, University of Virginia School of Medicine, Charlottesville, VA 22908, USA
    Brain Res 942:120-3. 2002
    ..After 8-24 h at room temperature and overnight refrigeration gene expression correlation and equivalency declined, but 90-95% of detected genes were within +/-40% of baseline levels. Brain homogenate pH did not change with PMI...

Research Grants7

  1. OXIDATIVE STRESS IN PARKINSON'S DISEASE
    James Bennett; Fiscal Year: 2000
    ..Paradigms for evaluating neuroprotective therapies will also be developed to allow targeted approaches to correcting consequences of increased oxidative stress in cells. ..
  2. OXIDATIVE STRESS IN PARKINSON'S DISEASE
    James Bennett; Fiscal Year: 2001
    ..Paradigms for evaluating neuroprotective therapies will also be developed to allow targeted approaches to correcting consequences of increased oxidative stress in cells. ..
  3. OXIDATIVE STRESS IN PARKINSON'S DISEASE
    James Bennett; Fiscal Year: 2001
    ..Paradigms for evaluating neuroprotective therapies will also be developed to allow targeted approaches to correcting consequences of increased oxidative stress in cells. ..
  4. OXIDATIVE STRESS IN PARKINSON'S DISEASE
    James Bennett; Fiscal Year: 2002
    ..Paradigms for evaluating neuroprotective therapies will also be developed to allow targeted approaches to correcting consequences of increased oxidative stress in cells. ..
  5. OXIDATIVE STRESS IN PARKINSON'S DISEASE
    James Bennett; Fiscal Year: 2002
    ..Paradigms for evaluating neuroprotective therapies will also be developed to allow targeted approaches to correcting consequences of increased oxidative stress in cells. ..
  6. OXIDATIVE STRESS IN PARKINSON'S DISEASE
    James Bennett; Fiscal Year: 2003
    ..Paradigms for evaluating neuroprotective therapies will also be developed to allow targeted approaches to correcting consequences of increased oxidative stress in cells. ..
  7. OXIDATIVE STRESS IN PARKINSON'S DISEASE
    James Bennett; Fiscal Year: 2004
    ..Paradigms for evaluating neuroprotective therapies will also be developed to allow targeted approaches to correcting consequences of increased oxidative stress in cells. ..