Nahuai Badiola

Research interests

I am currently working in the discovery of new targets for Alzheimer’s Disease (AD). In our lab we recently described the biggest AD interactome(Soler et al. 2010), including several new interactions. Now we are working with cellular and animal models to unravel which of the novel interactions are relevant in AD pathology.

Previous working experience

2011-Present: Post-doctoral fellow at the Structural Bioinformatics and Network Biology Lab in the Institute for Research in Biomedicine (IRB), Barcelona, Spain.

2009-2011: Post-doctoral fellow at Alzheimer’s Laboratory in Sant Pau Hospital, Barcelona, Spain.

2005-2008: PhD in Molecular Biology and Biochemistry in Medicine Faculty of the Autonomous University of Barcelona (UAB), Barcelona, Spain with a short stay at the Neuroscience Institute, Goteborg University, Goteborg, Sweden.

2003-2005: MSc in Molecular Biology and Biochemistry in Medicine Faculty of the Autonomous University of Barcelona (UAB), Barcelona, Spain.

Publications

Soler-Lopez M, Badiola N, Zanzoni A, Aloy P Towards Alzheimer's root cause: ECSIT as an integrating hub between oxidative stress, inflammation and mitochondrial dysfunction: Hypothetical role of the adapter protein ECSIT in familial and sporadic Alzheimer's disease pathogenesis , Bioessays 2012, doi: 10.1002/bies.201100193 [link]

Barneda-Zahonero B, Servitja JM, Badiola N, Miñano-Molina AJ, Fadó R, Saura CA, Rodríguez-Alvarez J. Nurr1 Protein Is Required for N-Methyl-D-aspartic Acid (NMDA) Receptor-mediated Neuronal Survival, JBC 2012, doi: 10.1074/jbc.M111.272427 [link]

Badiola N, de Oliveira RM, Herrera F, Guardia-Laguarta C, Gonçalves SA, Pera M, Suárez-Calvet M, Clarimon J, Outeiro TF, Lleó A.Tau Enhances α-Synuclein Aggregation and Toxicity in Cellular Models of Synucleinopathy, PLoS ONE 2011, doi: 10.1371/journal.pone.0026609 [link]

Badiola N, Penas C, Miñano-Molina A, Barneda-Zahonero B, Fadó R, Sánchez-Opazo G, Comella JX, Sabriá J, Zhu C, Blomgren K, Casas C, Rodríguez-Alvarez J.Induction of ER stress in response to oxygen-glucose deprivation of cortical cultures involves the activation of the PERK and IRE-1 pathways and of caspase-12, Cell Death & Disease 2011, doi:10.1038/cddis.2011.31 [link]

Badiola N, Suárez-Calvet M, Lleó A. Tau phosphorylation and aggregation as a therapeutic target in tauopathies, CNS & Neurological Disorders-Drug Targets 2010, ISSN: 1871-5273 [link]

Barneda-Zahonero B, Miñano-Molina A, Badiola N, Fadó R, Xifró X, Saura CA, Rodríguez-Alvarez J. Bone morphogenetic protein-6 promotes cerebellar granule neurons survival by activation of the MEK/ERK/CREB pathway, Molecular Biology of the Cell 2009, doi:10.1091/mbc.E09-05-0424 [link]

Badiola N*, Malagelada C*, Llecha N, Hidalgo J, Comella JX, Sabriá J, Rodríguez-Alvarez J Activation of caspase-8 by tumour necrosis factor receptor 1 is necessary for caspase-3 activation and apoptosis in oxygen-glucose deprived cultured cortical cells, Neurobiology of Disease 2009, doi:10.1016/j.nbd.2009.06.005 [link]

Gozzelino R, Sole C, Llecha N, Segura MF, Moubarak RS, Iglesias-Guimarais V, Perez-Garcia MJ, Reix S, Zhang J, Badiola N, Sanchis D, Rodriguez-Alvarez J, Trullas R, Yuste VJ, Comella JX BCL-XL regulates TNF-alpha-mediated cell death independently of NF-kappaB, FLIP and IAPs, Cell Research 2008, doi:10.1038/cr.2008.76 [link]

Segura MF, Sole C, Pascual M, Moubarak RS, Perez-Garcia MJ, Gozzelino R, Iglesias V, Badiola N, Bayascas JR, Llecha N, Rodriguez-Alvarez J, Soriano E, Yuste VJ, Comella JX The long form of fas apoptotic inhibitory molecule is expressed specifically in neurons and protects them against death receptor-triggered apoptosis, Journal of Neuroscience 2007, doi:10.1523/JNEUROSCI.3462-07.2007 [link]

Malagelada C, Xifró X, Badiola N, Sabrià J, Rodríguez-Alvarez J. Histamine H2-receptor antagonist ranitidine protects against neural death induced by oxygen-glucose deprivation, Stroke 2004, doi:10.1161/01.STR.0000141160.66818.24 [link]

* Equal contribution