Brain diseases might be caused by a myriad of genetic and epigenetic factors that lead to neuronal dysfunction and death. There are currently no effective therapies to stop the neurodegenerative process and the available treatments are only symptomatic, with moderate efficiency. In the last decades several molecular tools emerged together with efficient delivery systems that allow modulating gene expression in the brain, raising new perspectives for gene therapy approaches for neurological diseases.

Our lab is currently testing novel therapeutic strategies to tackle neurodegenerative processes, particularly those involved in tauopathies and Parkinson’s disease. We use viral vectors to modulate the expression and post-transcriptional processing of candidate genes related to neurodegeneration. We analyse neuronal survival and functionality in vitro, using primary cultures and differentiated human neurons. We test phenotypic rescue in vivo performing studies in transgenic mice that model neurodegenerative diseases.

Lab Members

Lic. Sonia Espíndola
Ph.D. student 2014-2018
Fellow CONICET
soniaespindola@gmail.com

Lic. Manuela Sartor
Ph.D. student 2017-2021
Fellow CONICET

Ana Damianich
Ph.D. student 2016-2020
Fellow CONICET
adamianich@gmail.com

Publications

Tau isoforms imbalance impairs the axonal transport of the amyloid precursor protein (APP) in human neurons.
Lacovich V, Espindola SL, Alloatti M, Pozo Devoto V, Cromberg L, Čarná M, Forte G, Gallo JM, Bruno L, Stokin G, Avale ME*, Falzone TL*. 2017.
Journal of Neuroscience. 37:58-69. (*corresponding author)

Trans-splicing correction of tau isoform imbalance in a mouse model of tau mis-splicing.
Avale ME, Rodríguez-Martín T, Gallo JM. 2013.
Human Molecular Genetics. 22:2603-11.

Prefrontal nicotinic receptors control novel social interaction between mice.
Avale ME, Chabout J, Pons S, De Chaumont F, Olivo-Marin JC, Maskos U, Changeux JP and Granon S. 2011.
FASEB J. 2145-55.

Interplay of Beta2*nicotinic receptors and dopaminergic pathways in the control of locomotion
Avale ME, Faure P, Pons S, Granon S, Deltheil T, David D, Gardier A, Changeux JP, Maskos U.
Proc Natl Acad Sci USA. 105:15991-6. 2008.

The dopamine D4 receptor is essential for hyperactivity and impaired behavioral inhibition in a mouse model of attention deficit/hyperactivity disorder.
Avale ME, Falzone T, Gelman D, Low M, Grandy D, Rubinstein M. 2004.
Molecular Psychiatry. 9:718-26.

Maria Elena Avale

  • Antecedentes
  • 1999. Licenciada en Ciencias Biológicas , Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires.
  • 2004. Doctora en Ciencias Biológicas, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires.
  • 2005 – 2008. Postdoctorado en Instituto Pasteur de Paris, Francia.
  • 2009 – 2012. Postdoctorado en King’s College London, Reino Unido.
  • 2010 – 2012. Master (PGCAP) en Educación Superior, King’s College London, Reino Unido.
  • 2013 – actualidad. Investigadora Adjunta CONICET.
  • 2016 – actualidad. Jefa de Trabajos Prácticos, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires.