Research Topics
| Magali DumontSummaryAffiliation: Cornell University Country: USA Publications
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Publications
Neuroprotective strategies involving ROS in Alzheimer diseaseMagali Dumont
Department of Neurology and Neuroscience, Weill Cornell Medical College, New York, NY 10065, USA
Free Radic Biol Med 51:1014-26. 2011..Nonetheless, there is still hope for improved compounds that would better target pathways implicated in ROS production. In fact, facilitating the endogenous antioxidant system by modulating transcription has great promise for AD therapy...- Bezafibrate administration improves behavioral deficits and tau pathology in P301S miceMagali Dumont
Department of Neurology and Neuroscience, Weill Cornell Medical College, New York, NY 10065, USA
Hum Mol Genet 21:5091-105. 2012..Bezafibrate is therefore a promising agent for the treatment of neurodegenerative diseases associated with tau pathology... 
Behavioral phenotyping of mouse models of neurodegenerationMagali Dumont
Department of Neurology and Neuroscience, Weill Cornell Medical College, New York, NY, USA
Methods Mol Biol 793:229-37. 2011..A list of procedures is provided to evaluate motor skills for the study of ALS, HD, and PD models, and to evaluate spatial learning and memory for the study of AD models...- Behavioral deficit, oxidative stress, and mitochondrial dysfunction precede tau pathology in P301S transgenic miceMagali Dumont
Weill Cornell Medical College, Department of Neurology and Neuroscience, 525 East 68th St, Rm A569A, New York, NY 10065, USA
FASEB J 25:4063-72. 2011..At that age, mitochondria proteome deregulation became more apparent in male P301S mitochondria. The data strongly suggest that oxidative stress and mitochondrial abnormalities appear prior to tau pathology... - Apocynin administration does not improve behavioral and neuropathological deficits in a transgenic mouse model of Alzheimer's diseaseMagali Dumont
Weill Cornell Medical College, Department of Neurology and Neuroscience, 525 East 68th Street, New York, NY 10065, USA
Neurosci Lett 492:150-4. 2011..Also, the reduction of NOX-mediated oxidative stress may not be sufficient to prevent AD, since other sources of reactive oxygen species such as mitochondria may be more important... - Triterpenoid CDDO-methylamide improves memory and decreases amyloid plaques in a transgenic mouse model of Alzheimer's diseaseMagali Dumont
Department of Neurology and Neuroscience, Weill Cornell Medical College, New York, New York 10065, USA
J Neurochem 109:502-12. 2009..CDDO-MA was provided with chow (800 mg/kg) from 1 to 4 months of age. CDDO-MA significantly improved spatial memory retention and reduced plaque burden, Abeta42 levels, microgliosis, and oxidative stress in Tg19959 mice... - Mitochondrial dihydrolipoyl succinyltransferase deficiency accelerates amyloid pathology and memory deficit in a transgenic mouse model of amyloid depositionMagali 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... - Coenzyme Q10 decreases amyloid pathology and improves behavior in a transgenic mouse model of Alzheimer's diseaseMagali Dumont
Department of Neurology and Neuroscience, Weill Cornell Medical College, New York, NY 10065, USA
J Alzheimers Dis 27:211-23. 2011..Our results show decreased pathology and improved behavior in transgenic AD mice treated with the naturally occurring antioxidant compound CoQ10. CoQ10 is well tolerated in humans and may be promising for therapeutic trials in AD... - Effects of synaptic modulation on beta-amyloid, synaptophysin, and memory performance in Alzheimer's disease transgenic miceDavide Tampellini
Department of Neurology and Neuroscience, Weill Cornell Medical College, New York, New York 10065, USA
J Neurosci 30:14299-304. 2010..These data support beneficial effects of synaptic activation on Aβ-related synaptic and behavioral impairment in AD... - N-iminoethyl-L-lysine improves memory and reduces amyloid pathology in a transgenic mouse model of amyloid depositionMagali Dumont
Weill Cornell Medical College, Department of Neurology and Neuroscience, New York, NY 10065, USA
Neurochem Int 56:345-51. 2010..These findings are consistent with previous reports demonstrating that iNOS inhibition ameliorates AD pathogenesis... - Reduction of oxidative stress, amyloid deposition, and memory deficit by manganese superoxide dismutase overexpression in a transgenic mouse model of Alzheimer's diseaseMagali Dumont
Weill Cornell Medical College, Department of Neurology and Neuroscience, 525 E 68th St, New York, NY 10065, USA
FASEB J 23:2459-66. 2009.... - Behavioral improvement after chronic administration of coenzyme Q10 in P301S transgenic miceCeyhan Elipenahli
Weill Cornell Medical College, Department of Neurology and Neuroscience, New York, NY, USA
J Alzheimers Dis 28:173-82. 2012..Our data show that coenzyme Q10 significantly improved behavioral deficits and survival in transgenic mice with the P301S tau mutation, upregulated key enzymes of the electron transport chain, and reduced oxidative stress... - Triterpenoids CDDO-ethyl amide and CDDO-trifluoroethyl amide improve the behavioral phenotype and brain pathology in a transgenic mouse model of Huntington's diseaseCliona Stack
Department of Neurology and Neuroscience, Weill Cornell Medical College, 525 East 68th Street, New York, New York 10065, USA
Free Radic Biol Med 49:147-58. 2010..They also rescued striatal atrophy in the brain and vacuolation in the brown adipose tissue. Therefore compounds targeting the Nrf2/ARE pathway show great promise for the treatment of HD... - Resveratrol protects against peripheral deficits in a mouse model of Huntington's diseaseDaniel J Ho
Weill Cornell Medical College, Department of Neurology and Neuroscience, 525 E 68th Street, New York, NY 10065, USA
Exp Neurol 225:74-84. 2010..Activation of the PGC-1alpha signaling pathway via resveratrol-induced activation of SIRT1, therefore, is an effective therapy in BAT, but not in the central nervous system of HD transgenic mice... - Mitochondria and antioxidant targeted therapeutic strategies for Alzheimer's diseaseMagali Dumont
Weill Cornell Medical College, Department of Neurology and Neuroscience, New York, NY, USA
J Alzheimers Dis 20:S633-43. 2010..Upregulation of antioxidant gene expression was beneficial in mice, giving hope for future avenues in the treatment of AD and other neurodegenerative disorders... - In vivo pathogenic role of mutant SOD1 localized in the mitochondrial intermembrane spaceAnissa Igoudjil
Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York, New York 10065, USA
J Neurosci 31:15826-37. 2011.... - Synaptic activity reduces intraneuronal Abeta, promotes APP transport to synapses, and protects against Abeta-related synaptic alterationsDavide Tampellini
Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York, New York 10065, USA
J Neurosci 29:9704-13. 2009.... - Behavioral deficits and progressive neuropathology in progranulin-deficient mice: a mouse model of frontotemporal dementiaFangfang Yin
Department of Microbiology and Immunology, Weill Cornell Medical College, New York, NY 10065, USA
FASEB J 24:4639-47. 2010..Thus, progranulin deficiency induced FTD-like behavioral and neuropathological deficits. These mice may serve as an important tool for deciphering underlying mechanisms in frontotemporal dementia...