Jose Rodriguez-Alvarez

Jose Rodriguez-Alvarez, Ph.D.

Area of research

  • Mechanisms involved in synaptic dysfunction and neuronal death in neurodegenerative diseases.

Email

Phone

Location

  • Albert Einstein College of Medicine Rose F. Kennedy Center 1410 Pelham Parkway South 701 Bronx, NY 10461


Professional Interests

Multiple evidences have supported a role for beta amyloid (Aβ) in the aetiology and pathogenesis of AD. It is believed that the progressive accumulation of self-aggregates of Aβ as oligomers (oAβ) would mediate synaptic dysfunction, leading to the initial cognitive deficits observed in MCI and earlier AD stages. At present, my principal interest is the study of the mechanisms involved in the alteration of synaptic activity and learning and memory dysfunction associated to early stages in Alzheimer’s disease as a way to identify novel therapeutic targets and biomarkers for earlier diagnosis and functional recovery. In particular, we are exploring the altered regulation of functional synaptic AMPA receptors in experimental AD models by a combination of different processes including transcriptional and post-transcriptional gene regulation, changes in AMPA receptors regulatory proteins or alteration in the neuromuscular unit affecting the release of angineurins.

Selected Publications

Català-Solsona, J, Miñano-Molina, AJ & J. Rodríguez-Alvarez.

Nr4a2 trasncription factor in hippocampal synaptic plasticity, memory and cognitive dysfunction. Front. Mol. Neurosci. 14:786226 (2021). doi: 10.3389/fnmol.2021.786226.

 

Siedlecki-Wullich D, Miñano-Molina AJ & J Rodriguez-Alvarez. microRNAs as early biomarkers of Alzheimer’s disease: A synaptic perspective. Cells 2021, 10, 113. doi.org/10.3390/cells10010113

 

Cheng W, Siedlecki-Wullich D, Catala-Solsona J, Fabregas C, Fadó R., Casals N, Sole M, Unzeta M, Saura C.A, Rodríguez-Alvarez J & AJ Miñano-Molina. Proteosomal-dependent AKAP150 degradation accompanies AMPAR endocytosis during cLTP. 

eNeuro 23 March 2020, 7 (2) ENEURO.0218-19.2020

 

Siedlecki-Wullich D, Catala-Solsona J, Fabregas C, Hernandez I, Clarimon J, Lleó A, Boada M, Saura CA, Rodriguez-Alvarez J and Miñano-Molina AJ. Alteration of microRNAs related to synaptic function as potential plasma biomarkers for Alzheimer disease. Alzheimer Res & Ther 11:46 (2019)

 

Parra-Damas, A., Chen, M., Enríquez-Barreto, L., Ortega, L., Acosta, S., Camats, J., Fullana, N., Aguilera, J., Rodríguez-Alvarez, J & C.A. Saura. CRTC1 function during memory encoding is disrupted in neurodegeneration. Biol Psychiatry  81:111-123 (2017)

 

Fado R., Soto D., Miñano-Molina A., Pozo M., Carrasco P., Yefimenko N., Rodríguez-Alvarez J & Casals N. Specific regulation of GluA subunit synthesis and AMPA receptor-mediated synaptic function by CPT1C in the hippocampus. J Biol Chem 290:25548-25560 (2015) 

 

Parra-Damas, A., Valero, J., Chen, M., España, J., Martín, E., Ferrer, I., Rodríguez-Alvarez, J & C.A. Saura. CRTC1 activates a transcriptional program deregulated at early Alzheimer’s disease-related stages. J Neurosci. 34:5576-5787 (2014)

 

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) 

 

Miñano-Molina, A.J., España, J., Martin, E. Barneda-Zahonero, B., Fadó, R., Solé M., Trullás, R., Saura, C.A. & J. Rodríguez-Alvarez. Soluble oligomers of amyloid-beta peptide disrupt AMPA receptors membrane trafficking contributing to early synapse dysfunction. J Biol. Chem. 286:27311-27321 (2011)

 

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)