Nélio Gonçalves
+351 239 820 190
Group at CNC

2014 --- Conducting post-doctoral research at the Center for Neuroscience and Cell Biology (Coimbra, Portugal) in Biomedicine domain, particularly on "Aging, Stress and Chronic Diseases: From Mechanisms to Therapeutics" and on “New Treatments for Stress-induced Dysregulation of Circuits Regulating Reward, Fear, and Habit Learning”, funded by FCT (PT), NAF (USA), DARPA (USA), and FEDER - QREN (EU);
2007 - 2013 - PhD in Pharmaceutical Biotechnology by the Faculty of Pharmacy, University of Coimbra, Portugal
2001 - 2007 - Licenciate in Pharmaceutical Sciences by FFUC, Portugal.

- 8 publications in high impact international peer-reviewed journals (all in Q1): Ann Neurol (2013), Mol Psychiatry (2014), Hum Mol Genet (2015 & 2014), J Neuroinflammation (2013), Front Cell Neurosci (2016) Radiother Oncol (2013) and Brain (2012);
- 4 publications in Conference Proceedings;
- 24 oral communications and 29 poster presentations in national and international scientific meetings.

- Doctoral Programmes: in Experimental Biology and Biomedicine (PDBEB-CNC, UC), and in Health Sciences (Faculty of Medicine, UC);
- Master’s degree in Pharmaceutical Biotechnology (FFUC);
- Supervisor of 1 completed Master Thesis in Biochemistry (FCTUC), 1 ongoing Master Thesis in Biomedical Research (FMUC); and 1 BSc traineeship in Molecular and Cell Biology (FCTUC)



Area of Research: 

Neurological and psychiatric disorders are multifactorial complex diseases of unknown etiopathogenesis. Combining expertise in the fields of molecular biology, biochemistry, cell biology, electrophysiology and imaging will hopefully identify selective brain regions and clarify circuit basis of dysfunction. Since the manipulation of a neuromodulation system operated by adenosine A2A receptors (A2AR) demonstrated to be effective controlling and alleviating different brain diseases, my focus range from elucidating the molecular and cellular mechanisms directly implicating A2AR in brain diseases to designing novel tools aiming at developing successful strategies to modify or block disease progression.

Research Summary: 
Selected Publications: 

1. Optogenetic activation of intracellular adenosine A2A receptor signaling in hippocampus is sufficient to trigger CREB phosphorylation and impair memory. Molecular Psychiatry (2015) DOI: 10.1038/mp.2014.182. Impact factor: 15.15

2. Neuropeptide Y mitigates neuropathology and motor deficits in mouse models of MJD. Human Molecular Genetics (2015) DOI: 10.1093/hmg/ddv271. Impact factor: 6.39

3. Calpain inhibition reduces ataxin-3 cleavage alleviating neuropathology and motor impairments in mouse models of Machado-Joseph disease. Human Molecular Genetics (2014), 23(18):4932-44. DOI: 10.1093/hmg/ddu209. Impact factor: 7.69

4. Caffeine and adenosine A2A receptor inactivation decrease striatal neuropathology in a lentiviral-based model of Machado-Joseph disease. Annals of Neurology (2013), v. 73, n. 5, p. 655-666. DOI: 10.1002/ana.23866. Impact factor: 11.19 (Prémio artigo destaque 2014, pela Sociedade Portuguesa de Neurociências – SPN)

5. Calpastatin-mediated inhibition of calpains in the mouse brain prevents mutant ataxin 3 proteolysis, nuclear localization and aggregation, relieving Machado-Joseph disease. Brain (2012), v. 135, n. 8, p. 2428-2439. DOI:10.1093/brain/aws177. Impact factor: 10.87 (Prémio Artigo Destaque 2013, SPN)

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