Maria Alexandra Brito

ORCID: 0000-0002-8493-4649
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About
Contact & Profiles
Research Areas
  • Neonatal Health and Biochemistry
  • Heme Oxygenase-1 and Carbon Monoxide
  • Barrier Structure and Function Studies
  • Erythrocyte Function and Pathophysiology
  • Neonatal and fetal brain pathology
  • Brain Metastases and Treatment
  • Drug Transport and Resistance Mechanisms
  • Neurological Disease Mechanisms and Treatments
  • Alzheimer's disease research and treatments
  • Methemoglobinemia and Tumor Lysis Syndrome
  • Glioma Diagnosis and Treatment
  • Cancer Cells and Metastasis
  • Metabolism and Genetic Disorders
  • X-ray Diffraction in Crystallography
  • Hemoglobinopathies and Related Disorders
  • Crystallization and Solubility Studies
  • Synthesis and Reactions of Organic Compounds
  • MicroRNA in disease regulation
  • Extracellular vesicles in disease
  • Caveolin-1 and cellular processes
  • Neuroscience and Neuropharmacology Research
  • Diabetes and associated disorders
  • Circular RNAs in diseases
  • Crystallography and molecular interactions
  • Biochemical Analysis and Sensing Techniques

University of Lisbon
2015-2024

Centro Hospitalar de Lisboa Central
2016-2020

Instituto de Medicina Molecular João Lobo Antunes
2018

Boca Raton Regional Hospital
2017

Central University of Venezuela
2010

Universidade do Porto
2008

Universidade Federal do Rio Grande do Sul
2006

Brazilian Agricultural Research Corporation
2005

University of Trieste
2000

Universidad Nacional Autónoma de México
1995

Age-related complications such as neurodegenerative disorders are increasing and remain cureless. The possibility of altering the progression or development these multifactorial diseases through diet is an emerging attractive approach with experimental support. We examined potential known bioavailable phenolic sulfates, arising from colonic metabolism berries, to influence hallmarks processes. In silico predictions in vitro transport studies across blood-brain barrier (BBB) endothelial...

10.1038/s41598-017-11512-6 article EN cc-by Scientific Reports 2017-09-07

The inflammatory mediator lipopolysaccharide (LPS) has been shown to induce acute gliosis in neonatal mice. However, the progressive effects on murine neurodevelopmental program over week that follows systemic inflammation are not known. Thus, we investigated of repeated LPS administration first postnatal mice, a condition mimicking sepsis late preterm infants, developing central nervous system (CNS).Systemic was induced by daily intraperitoneal (i.p.) (6 mg/kg) newborn mice from day (PND) 4...

10.1186/s12974-015-0299-3 article EN cc-by Journal of Neuroinflammation 2015-04-28

Abstract During neonatal hyperbilirubinaemia, astrocytes activated by unconjugated bilirubin (UCB) may contibute to brain toxicity through the production of cytokines. As a first step in addressing signal transduction cascades involved UCB‐induced astroglial immunological response, we tested whether tumour necrosis factor (TNF)‐α receptor 1 (TNFR1), mitogen‐activated protein kinase (MAPK) and nuclear κB (NF‐κB) would be exposed UCB, examined profile cytokine production. Astrocyte cultures...

10.1111/j.1471-4159.2006.03680.x article EN Journal of Neurochemistry 2006-02-10

Background Sepsis and jaundice are common conditions in newborns that can lead to brain damage. Though lipopolysaccharide (LPS) is known alter the integrity of blood-brain barrier (BBB), little on effects unconjugated bilirubin (UCB) even less joint UCB LPS microvascular endothelial cells (BMEC). Methodology/Principal Findings Monolayers primary rat BMEC were treated with 1 µg/ml and/or 50 µM UCB, presence 100 human serum albumin, for 4 or 24 h. Co-cultures astroglial cells, a more complex...

10.1371/journal.pone.0035919 article EN cc-by PLoS ONE 2012-05-07

Methamphetamine (METH) is a psychostimulant that causes neurologic and psychiatric abnormalities. Recent studies have suggested its neurotoxicity may also result from ability to compromise the blood–brain barrier (BBB). Herein, we show METH rapidly increased vesicular transport across endothelial cells (ECs), followed by an increase of paracellular transport. Moreover, triggered release tumor necrosis factor-alpha (TNF- α), blockade this cytokine or inhibition nuclear factor-kappa B (NF- κB)...

10.1038/jcbfm.2015.59 article EN Journal of Cerebral Blood Flow & Metabolism 2015-04-22

Ursodeoxycholic acid and its main conjugate glycoursodeoxycholic are bile acids with neuroprotective properties. Our previous studies demonstrated their anti-apoptotic, anti-inflammatory, antioxidant properties in neural cells exposed to elevated levels of unconjugated bilirubin (UCB) as severe jaundice. In a simplified model the blood-brain barrier, formed by confluent monolayers cell line human brain microvascular endothelial cells, UCB has shown induce caspase-3 activation death, well...

10.3389/fnins.2015.00080 article EN cc-by Frontiers in Neuroscience 2015-03-13

Phenolic compounds have been recognized as promising for the prevention of chronic diseases, including neurodegenerative ones. However, phenolics like flavan-3-ols (F3O) are poorly absorbed along gastrointestinal tract and structurally rearranged by gut microbiota, yielding smaller more polar metabolites phenyl-γ-valerolactones, phenylvaleric acids their conjugates. The present work investigated ability F3O-derived to cross blood-brain barrier (BBB), linking five experimental models with...

10.3390/nu11112678 article EN Nutrients 2019-11-05

Abstract When activated by unconjugated bilirubin (UCB), astrocytes are important sources of inflammatory mediators such as TNF‐α, IL‐1β and IL‐6, which may contribute for the neurotoxicity observed during severe neonatal hyperbilirubinemia. In present study, we have addressed role mitogen‐activated protein kinases (MAPKs) p38, Jun N‐terminal kinase (JNK)1/2 extracellular signal‐regulated (ERK)1/2 pathways their relation with nuclear factor κB (NF‐κB) cascade in signalling events involved...

10.1111/j.1460-9568.2007.05340.x article EN European Journal of Neuroscience 2007-02-01
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