MItochondria- & ExperieNce- Dependent neuronal plastIcity, NeurodeGeneration (MINDING)
Professeure - Université Toulouse III 05 61 55 62 38
- Noélie DAVEZAC
- Marie-Christine MIQUEL
- Laetitia PELLOQUIN-ARNAUNE
- Djamaa ATAMENA
- Marlène BOTELLA
- Aude DELEAU
- Manon MARQUE
- Tanoe Franck Eric GNANKOU
- Venu GURRAM
A mitochondrial gate to neuronal plasticity and neurodegeneration.
Finely tuned mitochondrial functions, from energy supply to cell homeostasis, are vital for highly specialized and energy-demanding cells, like neurons. A precise dynamics of mitochondrial fusion and fission events underlies their quality control and adaptability to cellular needs. As an illustration, pathologies directly associated to mutations in key fusion proteins, like Type 1 Dominant Optic Atrophy (OPA1 mutation), are mainly neurodegenerative. Reciprocally, progressive neurodegenerative diseases such as Alzheimer’s are linked not only to impairments of mitochondrial functions (energy, oxidative stress) but also to impairments of mitochondrial dynamics and turn-over.
Mainly centered on in vitro and in vivo DOA models, our projects aim at deciphering, and in fine modeling, the mechanisms of mitochondrial impact on neuronal homeostasis and synaptic plasticity. Spanning from adult neurogenesis to axonal degeneration, we also want to understand the impact of mitochondrial morphological and functional plasticity on experience-dependent neuronal plasticity and complex brain functions such as animal cognition.
- Claire Rampon, Lionel Mouledous, Sébastien Lopez (CBI-CRCA), Camille Lejards (CBI-CRCA),
- Raffele Leva (CBI-LMGM),
- Joel Bordeneuve-Guibé (ISAE-Supaero, Toulouse),
- Daniel Dunia (CPTP, Toulouse),
- Jean-Michel Peyrin (IBPS, Paris),
- Pascal Reynier (CHU Angers, France),
- Laurent Roybon (Lundt, Sweden),
- Bernd Wissinger (U. Tubingen, Germany)
Protective potential of the X protein in DOA (DOAX)
Mitophagy or Apoptosis: a choice Made in neurons by Bnip3-Opa1 interaction ? (MAMBO)
Mitochondria and Axonal degeneration in DOA: a story of shape and function.
MOdeling to predict the eVolution and trEatment of dominant Optic atrophy and OPA1 gene deficit related diseases pathogenesis (MOVE ONE) & identification of Reactive Oxygen Species and opA1 (ROSA)
Mitochondria, adult neurogenesis & learning and memory (MITOGATE)
- Daloyau M, Millet A.M.C., Miquel MC, Mils V., Wissinger B., Belenguer P ans Davezac N..
Brains from aged OPA1 +/- (B6;C3-Opa1 329-355del) mouse strain are in a pro-oxidative state
Reactive Oxygen Species
- Arrázola MS, Andraini T, Szelechowski M, Mouledous L, Arnauné-Pelloquin L, Davezac N, Belenguer P, Rampon C, Miquel MC..
Mitochondria in Developmental and Adult Neurogenesis
- Richetin K, Moulis M, Millet A, Arràzola MS, Andraini T, Hua J, Davezac N, Roybon L, Belenguer P, Miquel* MC, Rampon* C.
Amplifying mitochondrial function rescues adult neurogenesis in a mouse model of Alzheimer’s disease
Neurobiol Dis. 2017 Jun;102:113-124. doi: 10.1016.
2017 Jun in collaboration with Remember team
- Merabet N, Bordeneuve-Guibe J, Davezac N..
Modelling the redox imbalance in Dominant Optic Atrophy: the case of respiratory Complex I.
- Millet A., Merabet N., Bertholet A., Daloyau M., Reynier P., Galinier A., Devin Anne, Wissinger B, Bordeneuve-Guibe J., Belenguer P, Davezac N..
Imbalance of the REDOX state in dominant Optic Atrophy: the way of mathematical modeling.
Archives of the International Society of Antioxidants in Nutrition and Health (ISANH), Vol. 5, Issue 1, 2017.
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- Macarena S. Arrazola (Post-doct 2016; post-doct U. Santiago, Chile),
- Trinovita Andraini (PhD 2017; Assistant Professor, Physiology Department, U. Indonesia, Jakarta),
- Manon Moulis (PhD 2016; post-doc CHU Rangueil Toulouse),
- Thomas Delerue (PhD 2015; post-doc NIH Washington DC, USA),
- Aurélie Millet (PhD 2014); post-doc UCL),
- Ambre Bertholet (PhD 2011; post-doc UCSF, USA),
- Alan Diot (PhD 2011; post-doc Cambridge UK, ENS Lyon),
- Farnoosh Khosrobakhsh (PhD 2010; Assistant Professor, U. of Kurdistan, Iran).