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| First Name: | Magali | | Last Name: | Dumont | | Title: | Assistant Professor in Neuroscience | | Advanced Degrees: | Ph.D. | | Affiliation: | Weill Cornell Medical College | | Department: | Neurology and Neuroscience | | Street Address 1: | 1300 York Avenue | | Street Address 2: | Room A578 | | City: | NY | | State/Province: | NY | | Zip/Postal Code: | 10065 | Country/Territory: | U.S.A. | | Phone: | 212 746 4818 | | Email Address: |  |
Disclosure:
(view policy)
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Member reports no financial or other potential conflicts of interest. [Last Modified: 15 August 2010]
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View all comments by Magali Dumont
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Aging Process, Alzheimer Disease
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Oxidative Stress, Animal Models, A-beta PP/A-beta, Neurobiology
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1.Lalonde R., Dumont M., Staufenbiel M., Sturchler-Pierrat C. & Strazielle C. (2002). Spatial learning, exploration, anxiety, and motor coordination in female APP23 transgenic mice with the Swedish mutation. Brain Res. 956, 36-44
2.Lalonde R., Dumont M., Fukuchi K. & Strazielle C. (2002). Transgenic mice expressing the human C99 terminal fragment of beta-APP: Effects on spatial learning, exploration, anxiety, and motor coordination. Exp. Gerontol. 37,1399-1410
3.Dumont M., Strazielle C., Staufenbiel M. & Lalonde R. (2004). Spatial learning and exploration of environmental stimuli in 24-month-old female APP23 transgenic mice with the Swedish mutation. Brain Res. 1024, 113-121
4.Dumont M., Lalonde R., Ghersi-Egea J.-F., Fukuchi K. & Strazielle C. (2006). Regional acetylcholinesterase activity and its correlation with behavioral performances in transgenic mice expressing the human C99 fragment of APP. J. Neural Transm. 113, 1225-1241
Neuroscience 153, 986-996
5.Dumont M., Wille E., Calingasan N.Y., Tampellini D., Williams C., Gouras G.K., Liby K., Sporn M., Beal M.F. & Lin M.T. (2009). Triterpenoid CDDO-methylamide improves memory and decreases amyloid plaques in a transgenic mouse model of Alzheimer’s disease. J. Neurochem. 109, 502-512
6.Dumont M., Wille E., Stack C., Calingasan N., Beal M.F. & Lin M.T. (2009). Reduction of oxidative stress, amyloid deposition, and memory deficit by manganese superoxide dismutase overexpression in a transgenic mouse model of Alzheimer’s disease. FASEB J. 23, 2459-2466
7.Tampellini D., Rahman N., Gallo E., Huang Z., Dumont M., Capetillo-Zarate E., Ma T., Zheng R., Lu B., Nanus D., Lin M. & Gouras, G.K. (2009). Synaptic activity reduces intraneuronal A-beta, promotes APP transport to synapses and protects against A-beta-related synaptic alterations. J. Neurosci. 29, 9704-9713
8.Dumont M.*, Ho D., Calingasan N.Y., Xu H., Gibson G. & Beal M.F. (2009). Mitochondrial dihydrolipoyl succinyltransferase deficiency accelerates amyloid pathology and memory deficit in transgenic Alzheimer mice. Free Rad. Biol. Med. 47, 1019-1027
9.Dumont M., Wille E., Calingasan N.Y., Nathan C., Beal M.F. & Lin M.T. (2009). N-Iminoethyl-L-Lysine improves memory and reduces amyloid pathology in a transgenic mouse model of amyloid deposition. Neurochemistry Int. 56, 345-351
10.Stack C., Ho D., Wille E., Calingasan N.Y., Williams C., Liby K., Sporn M., Dumont M.* & Beal M.F. (2010). Triterpenoids CDDO-ethyl amide and CDDO-trifluoroethyl amide improve the behavioral phenotype and brain pathology in a transgenic mouse model of Huntington’s disease. Free Rad. Biol. Med. (in press)
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