Dora Brites

PhD (1988) in Pharmacy (Biochemistry), Universidade de Lisboa
Investigator Coordinator, Neurobiology, Biochemistry and Human Biology
iMed.ULisboa, Faculdade de Farmácia, Universidade de Lisboa

Faculdade de Farmácia, Universidade de Lisboa — Av. Prof. Gama Pinto, 1649-003 Lisboa, Portugal

T (+351) 217 946 450
F (+351) 217 946 491
Researcher ID M-8293-2013
Group Researcher ID B-5403-2014
Scopus Author ID 7004026610

Research Interests

The group headed by Brites investigates neuron-glia-vascular interactions and the role of secretome, inflammatory miRNA, exosomes and astrocyte/microglia phenotypic diversity in neuroinflammation-associated and demyelinating neurodegenerative diseases. Conventional (2D) and improved (3D) cellular models, as well as transdifferentiation and iPSCs reprogramming technologies using patient fibroblasts, are used to identify pathophysiological mechanisms, early biomarkers/targets, and to test reparative medicines/repurposing drugs for AD, MS and ALS.

Selected Publications

Cunha C, Santos C, Gomes C, Fernandes A, Correia AM, Sebastião AM, Vaz AR, Brites D. Downregulated glia interplay and increased miRNA-155 as promising markers to track early ALS stage. Mol Neurobiol 2018; 55: 4207-24.

Caldeira C, Cunha C, Vaz AR, Falcão AS, Barateiro A, Seixas E, Fernandes A, Brites D. Key aging-associated alterations in primary microglia response to beta-amyloid stimulation. Front Aging Neurosci 2017; 9: 277.

Pinto S, Cunha C, Barbosa M, Vaz AR, Brites D. Exosomes from NSC-34 Cells transfected with hSOD1-G93A are enriched in miR-124 and drive alterations in microglia phenotype. Front Neurosci 2017; 11: 273.

Falcão AS, Carvalho LA, Lidónio G, Vaz AR, Lucas SD, Moreira R, Brites D. Dipeptidyl vinyl sulfone as a novel chemical tool to inhibit HMGB1/NLRP3-inflammasome and inflamma-miRs in Aβ-mediated microglial inflammation. ACS Chem Neurosci 2017; 8: 89-99.

Barateiro A, Chen S, Yueh MF, Fernandes A, Domingues HS, Relvas J, Barbier O, Nguyen N, Tukey RH, Brites D. Reduced Myelination and Increased Glia Reactivity Resulting from Severe Neonatal Hyperbilirubinemia. Mol Pharmacol 2016; 89: 84-93.