ORCID Research Profile
ESTHER PÉREZ NAVARRO
Position: Associate Professor
Research team
Rafael Alcala Vida
Early stage researcher
Ana Saavedra Martins
Collaborator
Gloria Blazquez Romero
Collaborator
Jordi Creus Muncunill
Collaborator
Marta Garcia Forn
Collaborator
Contact details
Dr. Esther Pérez Navarro
Department of Biomedicine
Faculty of Medicine, Casanova 143
08036 Barcelona (Spain)
34 93 403 52 84
estherperez (at) ub.edu
Research Interests
The main objective of our group is to study molecular mechanisms that control motor coordination and cognitive function, with the main focus on the activity of kinases and phosphatases, and whether alterations in these mechanisms contribute to the symptoms observed in Huntington’s disease (HD). Although HD has been classically considered a motor disorder there is now considerable evidence that early cognitive deficits appear in patients before the onset of motor disturbances. Our final goal is thus to identify new therapeutic targets to ameliorate or prevent motor and cognitive dysfunction. We are also interested in studying whether alterations observed in the brain can be detected in blood samples from HD patients.
Current Research Lines
- Study of the involvement of the Striatal-Enriched Protein Tyrosine phosphatase (STEP) in motor control and cognitive function (motor learning, hippocampal-dependent learning and social memory)
- Analysis of the role of alterations in lamin levels (PKC delta target) in neuronal dysfunction in HD
- Study of aberrant protein translation as a new pathogenic mechanism in HD
Technologies / methods
- Behavioral assessment: Rotarod (fixed and accelerating); novel object recognition test; novel object location test, Morris water maze; vertical pole, balance beam, T-maze spontaneous alternation task, Open field, Dark-light box, Plus maze, SHIRPA battery, Three-chamber test of sociability and social novelty test, Five-trial social memory assay, Direct interaction test, Dominance tube, Resident-Intruder test, Buried food test and Olfactory habituation/dishabituation test.
- Stereotaxia, Western blot, cell fractionation, immunohistochemistry, stereology microscopy, morphological analysis, PCR, Cell culture (cell lines and neuronal primary cultures), transfection and infection.
Highlighted publications
· Rué L, Bañez-Coronel M, Creus-Muncunill J, Giralt A, Alcalá-Vida R, Mentxaka G, Kagerbauer B, Zomeño-Abellán MT, Aranda Z, Venturi V, Pérez-Navarro E, Estivill X, Martí E. Targeting CAG repeat RNAs reduces Huntington’s disease phenotype independently of huntingtin levels. J Clin Invest. 2016, 126:4319-4330.
· Azkona G, Saavedra A, Aira Z, Aluja D, Xifró X, Baguley T, Alberch J, Ellman JA, Lombroso PJ, Azkue JJ, Pérez-Navarro E. STEP modulates nociception: evidences from genetic deletion and pharmacological inhibition. Pain, 2016, 157:377-386
· Tyebji S, Saavedra A, Canas PM, Pliassova A, Delgado-García JM, Alberch J, Cunha RA, Gruart A, Pérez-Navarro E (2015) Hyperactivation of D1 and A2A receptors contributes to cognitive dysfunction in Huntington’s disease. Neurobiol Dis. 74:41-57.
· Saavedra A, Giralt A, Rué L, Xifró X, Xu J, Ortega Z, Lucas JJ, Lombroso PJ, Alberch J, Pérez-Navarro E (2011) Striatal-enriched protein tyrosine phosphatase expression and activity in Huntington’s disease: a STEP in the resistance to excitotoxicity. J Neurosci. 31:8150-62.
· Giralt A, Saavedra A, Carretón O, Xifró X, Alberch J, Pérez-Navarro E. (2011) Increased PKA signaling disrupts recognition memory and spatial memory: role in Huntington’s disease. Hum Mol Genet. 20:4232-4247.