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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Gary E. Gibson

Weill Cornell Medical College/Burke Medical Research Institute

White Plains

USA

[email]@med.cornell.edu

Name/email consistency: high

 
 
 
 
 
 
 

Affiliations

  • Weill Cornell Medical College/Burke Medical Research Institute, White Plains, USA. 1997 - 2010
  • Department of Neurology and Neurosciences, Weill Medical College of Cornell University, Burke Medical Research Institute, White Plains, USA. 1999 - 2010
  • Burke Medical Research Institute, Weil Medical College, Cornell University, 785 Mamaroneck Avenue, USA. 2002

References

  1. A mitocentric view of Alzheimer's disease suggests multi-faceted treatments. Gibson, G.E., Shi, Q. J. Alzheimers Dis. (2010) [Pubmed]
  2. Cause and consequence: mitochondrial dysfunction initiates and propagates neuronal dysfunction, neuronal death and behavioral abnormalities in age-associated neurodegenerative diseases. Gibson, G.E., Starkov, A., Blass, J.P., Ratan, R.R., Beal, M.F. Biochim. Biophys. Acta (2010) [Pubmed]
  3. Oxidant-induced changes in mitochondria and calcium dynamics in the pathophysiology of Alzheimer's disease. Gibson, G.E., Karuppagounder, S.S., Shi, Q. Ann. N. Y. Acad. Sci. (2008) [Pubmed]
  4. Thiamine-dependent processes and treatment strategies in neurodegeneration. Gibson, G.E., Blass, J.P. Antioxid. Redox Signal. (2007) [Pubmed]
  5. Foreword. Gibson, G.E. Neurochem. Res. (2007) [Pubmed]
  6. Oxidative stress in Alzheimer's disease. Gibson, G.E., Huang, H.M. Neurobiol. Aging (2005) [Pubmed]
  7. The alpha-ketoglutarate-dehydrogenase complex: a mediator between mitochondria and oxidative stress in neurodegeneration. Gibson, G.E., Blass, J.P., Beal, M.F., Bunik, V. Mol. Neurobiol. (2005) [Pubmed]
  8. Selective response of various brain cell types during neurodegeneration induced by mild impairment of oxidative metabolism. Ke, Z.J., Gibson, G.E. Neurochem. Int. (2004) [Pubmed]
  9. Deficits in a tricarboxylic acid cycle enzyme in brains from patients with Parkinson's disease. Gibson, G.E., Kingsbury, A.E., Xu, H., Lindsay, J.G., Daniel, S., Foster, O.J., Lees, A.J., Blass, J.P. Neurochem. Int. (2003) [Pubmed]
  10. Interactions of oxidative stress with thiamine homeostasis promote neurodegeneration. Gibson, G.E., Zhang, H. Neurochem. Int. (2002) [Pubmed]
  11. Oxidative processes in the brain and non-neuronal tissues as biomarkers of Alzheimer's disease. Gibson, G.E., Huang, H.M. Front. Biosci. (2002) [Pubmed]
  12. Oxidative stress increases internal calcium stores and reduces a key mitochondrial enzyme. Gibson, G.E., Zhang, H., Xu, H., Park, L.C., Jeitner, T.M. Biochim. Biophys. Acta (2002) [Pubmed]
  13. Interactions of oxidative stress with cellular calcium dynamics and glucose metabolism in Alzheimer's disease. Gibson, G.E. Free Radic. Biol. Med. (2002) [Pubmed]
  14. The alpha-ketoglutarate dehydrogenase complex in neurodegeneration. Gibson, G.E., Park, L.C., Sheu, K.F., Blass, J.P., Calingasan, N.Y. Neurochem. Int. (2000) [Pubmed]
  15. Differential alterations in antioxidant capacity in cells from Alzheimer patients. Gibson, G.E., Zhang, H., Sheu, K.R., Park, L.C. Biochim. Biophys. Acta (2000) [Pubmed]
  16. Oxidative stress and a key metabolic enzyme in Alzheimer brains, cultured cells, and an animal model of chronic oxidative deficits. Gibson, G.E., Park, L.C., Zhang, H., Sorbi, S., Calingasan, N.Y. Ann. N. Y. Acad. Sci. (1999) [Pubmed]
  17. Abnormalities in Alzheimer's disease fibroblasts bearing the APP670/671 mutation. Gibson, G.E., Vestling, M., Zhang, H., Szolosi, S., Alkon, D., Lannfelt, L., Gandy, S., Cowburn, R.F. Neurobiol. Aging (1997) [Pubmed]
 
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