Experimental therapeutics of Parkinson disease
Research center
Institution
Laboratory
Keywords
Publications
Rousseau E, Michel PP, Hirsch EC. The iron-binding protein lactoferrin protects vulnerable dopamine neurons from degeneration by preserving mitochondrial calcium homeostasis. Mol Pharmacol. 2013 Dec;84(6):888-98. doi: 10.1124/mol.113.087965. Epub 2013 Sep 27.
Karachi C, André A, Bertasi E, Bardinet E, Lehéricy S and Bernard F (2012) Functional parcellation of the lateral mesencephalus.JNeurosci. 32(27):9396-9401. (IF 7.27)ACL
Huynh MB, Villares J, Sepúlveda Díaz JE, Christiaans S, Carpentier G, Ouidja MO, Sissoeff L, Raisman-Vozari R, Papy-Garcia D (2012) Glycosaminoglycans from aged human hippocampus have altered capacities to regulate trophic factors activities but not A?42 peptide toxicity. Neurobiol Aging 33 (5), 1005.e11-22 (IF : 6.63)ACL
Dumurgier J, Crivello F, Mazoyer B, Tavernier B, Grabli D, François C, Tzourio-Mazoyer N, Tzourio C, Elbaz A (2012) Mri Atrophy Of The Caudate Nucleus And Slower Walking Speed In The Elderly: A Population-Based Study. Neuroimage 60 (2), 871-878(IF:5.94) ACL
Torres-Bugeau CM, Avila Cl, Raisman-Vozari R, Papy-Garcia D, Itri R, Barbosa Lr, Cortez Lm, Sim Vl, Chehin Rn (2012) Characterization of heparin-induced glyceraldehyde-3-phosphate dehydrogenase early amyloid-like oligomers and their implication on ?-synuclein aggregation. J Biol Chem 287: 2398-2409. (IF 5.33)ACL
Ribeiro N, Thuaud F, Bernard Y, Gaiddon C, Cresteil T, Hild A, Hirsch EC, Michel PP,•Nebigil CG,Desaubry L (2012) Flavaglines as Potent Anticancer and Cytoprotective Agents. J Med Chem (IF 5.25) ACL
Fields of research
Research Theme
Our project is driven by two major complementary objectives:
1) to characterize the mechanisms involved in the progression of nerve cell death in neurodegenerative disorders and especially Parkinson’s disease (PD);
2) to identify functional alterations underlying key clinical symptoms in these disorders. To that aim, we concentrate on the populations of dopaminergic (DA) and cholinergic neurons that are preferentially affected in PD. Our hope is to identify therapeutic targets to slow the progression of neuronal loss and to alleviate symptoms originating from non-DA lesions which represent two major unmet needs for patients suffering from PD. The main targets analyzed are oxidative stress, the role of calcium homeostasis, electrical activity and neuroinflammatory processes.