CV Science

Diana Zala PhD, The bioenergetics of neuronal plasticity

Course and current status

Current position  

 2019- Full time Researcher - CR1, Inserm

IPNP, Paris, France, in the group of Dr. Zsolt LENKEI 

   Research focus

• The bioenergetics of cytoskeletal dynamics

Professional experience

Since  - 2018- CRCN, Inserm

IPNP, Paris, France, in the group of Dr. Zsolt LENKEI

2015 - 2017- CR1, Inserm

ESPCI, Paris, France, in the group of Dr. Zsolt LENKEI

2012 - 2014 - CR1, Inserm

Institut Curie, Orsay, France, in the group of Dr. Frédéric SAUDOU 

2005-2012 - Postdoctoral scientist
 

Institut Curie, Orsay, France, in the group of Dr. Frédéric SAUDOU 

   Research focus

• Huntingtin fonction in axonal transport.

• To understand the link between ATP production and consummation in axonal transport.
• Restoring axonal transport as therapeutic strategies for Huntington's Disease.

1998-2004 - PhD student
Swiss Federal Institute of Technology of Lausanne (EPFL)
In the group of Dr Patrick AEBISCHER/Dr Nicole DEGLON

   Research focus

• Gene Therapy in Huntington's Disease.
• Modeling Huntington's Disease with lentiviral vectors.

Education

2005. PhD in Neurodegenerative Diseases
Brain and Mind Institute, Swiss Federal Institute of Technology of Lausanne (EPFL)

1998. Master of Chemical Engineering specialization in Biotechnology
The Institute of Chemical Sciences and Engineering, Swiss Federal Institute of Technology of Lausanne (EPFL)

Scientific summary

   Research interests

• Metabolism and Structural Plasticity
  
• Understand axonal transport in health and diseases.
• Restoring axonal transport in Neurodegenerative diseases.

   Main results

• Local glycolysis fuells axonla retraction (Santos et al., JCB 2023).
• Nanopaint: A Tool for Rapid and Dynamic Imaging of membrane Structural Plasticity at the Nanoscale (Tasso et al, Small 2019)
• Huntingtin scaffolds glycolytic enzymes on vesicles to produce on-board ATP (Zala et al., Cell 2013).
• Huntingtin fonction on axonal tranpsort is conserved in Drosophila melanogaster (Zala et al., PLoS One  2013).
• Huntingtin phosphorylation is restoring axonal transport in HD models (Zala et al., Hum Mol Genet  2008).
• Huntingtin phosphorylation is a molecular switch for vesicular directionality (Colin, Zala et al., EMBO J 2008).
• Development of a lentiviral-based cellular model of Huntington's disease ( Zala et al., Neurobiol Dis  2005).
• Assessment of the long term  lentiviral-mediated delivery of Ciliary Neurotrophic Factor (CNTF) in the striatum of transgenic HD mice ( Zala et al., Exp Neurol  2004).