Biomedical research group in Neurodegeneration REBINE



Coordinator: Dr. José Rodríguez Álvarez

- Dr. José Aguilera Ávila
- Dr. Carlos A. Saura Antolín
- Dr. José Rodríguez Álvarez



Our research group is interested in the mechanisms that control the synaptic dysfunction and neural death/survival in neurodegenerative diseases and other pathologies that occur with neuronal loss. During the last 10 years, our research has been focused on the study of the alterations in synaptic function and gene expression that could be responsible for the early changes in synaptic function and the cognitive decline during AD progression. A better knowledge of the events occurring in the early stages will, eventually, lead to the identification of promising targets for early therapeutical intervention and of biomarkers that could improve the early diagnosis of the disease.



Research lines:


1) Study the role of CRTC1-Nr4a2 axis on early synaptic disruption and cognitive impairment in AD


2) Identification of potential biomarkers  for early diagnosis of the disease.


3) Alteration of synaptic AMPA receptors function and transport in AD.


4) Study the role of CREB-CRTC1/2 on AD-mediated neurodegeneration.



Active projects:


- SAF2017-89271-R; Implicación de Nr4a2/Nurr1 en la disfunción sináptica y déficits cognitivos en fases tempranas de la Enfermedad de Alzheimer


- Proyectos CIBERNED; Estudio del microRNA en el compartimiento exosomal del líquido cefalorraquiodeo como biomarcador de la demencia fronto-temporal y herramienta para el reconocimiento de las bases biológicas de la enfermedad


- SAF2016-80027-R; Transcriptional mechanisms of synaptic plasticity in memory circuits in a mouse mouse of neurodegeneration

Ministerio de Economía y Competitividad


- Marato TV3 2013-343; Searching new biomarkers and therapeutic targets related to cognitive deficits in early stages of Alzheimer's Disease: Role of AKAP79/150, CPT1C and SSAO/VAP-1 in Ab-mediated AMPAR dysfunction.


- A2014417S; Transcriptional mechanisms of memory loss in Alzheimer’s disease





Featured publications:


- Parra-Damas A, Chen M, Enriquez-Barreto L, Ortega L, Acosta S, Perna JC, Fullana MN, Aguilera J, Rodríguez-Alvarez J, Saura CA. CRTC1 Function DuringMemory Encoding Is Disrupted in Neurodegeneration. Biol Psychiatry. 2017 Jan15;81(2):111-123. doi: 10.1016/j.biopsych.2016.06.025. Epub 2016 Jul 11. PubMedPMID: 27587263.


- Parra-Damas A, Valero J, Chen M, España J, Martín E, Ferrer I, Rodríguez-Alvarez J, Saura CA. Crtc1 activates a transcriptional programderegulated at early Alzheimer's disease-related stages. J Neurosci. 2014 Apr 23;34(17):5776-87. doi: 10.1523/JNEUROSCI.5288-13.2014. PubMed PMID: 24760838.


- Fadó, R., Moubarak, R., Miñano-Molina, A.J., Barneda-Zahonero, B., Valero, J., Saura, C.A., Morán, J., Comella, J.X. & J. Rodríguez-Alvarez.  X-linked inhibitor of apoptosis protein negatively regulates neurite outgrowth through interaction with cRAF and Trk. Sci. Reports 3:2397 (2013) doi: 10.1038/srep02397


- Barneda-Zahonero, B., Servitja, J.M., Badiola, N., Miñano-Molina, A.J., Fadó, R., Saura, C.A. & J. Rodriguez-Alvarez. Nurr1 is required for NMDA receptor-mediated neuronal survival. J. Biol. Chem. 287:11351-11362 (2012)


- España, J., Valero, J., Miñano-Molina, A., Masgrau, R., Martín,E., Guardia-Laguarta,C., Lleó, A., Giménez-Llort, L., Rodríguez-Alvarez, J. & C.A. Saura. β-amyloid disrupts activity-dependent gene transcription required for memory through the CREB coactivator CRTC1. J. Neurosci. 30:9402-9410 (2010)











Ref. SGR 2017-0749