A5076957410- Neuroinflammation and Neurodegeneration Mechanisms
- Neuroscience and Neuropharmacology Research
- Neuropeptides and Animal Physiology
- Neurogenesis and neuroplasticity mechanisms
- Receptor Mechanisms and Signaling
- Barrier Structure and Function Studies
- Neurotransmitter Receptor Influence on Behavior
- Memory and Neural Mechanisms
- Ion channel regulation and function
- Drug Transport and Resistance Mechanisms
- Epilepsy research and treatment
- Nerve injury and regeneration
- Sleep and Wakefulness Research
- Brain Metastases and Treatment
- Glioma Diagnosis and Treatment
- Immune cells in cancer
- Attention Deficit Hyperactivity Disorder
- Alzheimer's disease research and treatments
- Neurological Disorders and Treatments
- Chemokine receptors and signaling
- Adipose Tissue and Metabolism
- Traumatic Brain Injury and Neurovascular Disturbances
- Autism Spectrum Disorder Research
- Retinopathy of Prematurity Studies
- Cardiovascular, Neuropeptides, and Oxidative Stress Research
University of Coimbra
2015-2024
Hospital Center of Cova da Beira
2024
Grupo Santa Casa de Belo Horizonte
2024
Instituto Superior Técnico
2023
Association for Innovation and Biomedical Research on Light and Image
2007-2017
Institute of Pharmacology
2006-2017
Hospital de Santo António
2015
Centro Hospitalar do Porto
2015
Centro de Neurociências e Biologia Celular
2006-2007
Cell2B (Portugal)
2005
Myocardial infarction (MI) is the leading cause of morbidity and mortality worldwide results from an obstruction in blood supply to a region heart. In attempt replenish oxygen nutrients deprived area, affected cells release signals promote development new vessels confer protection against MI. However, mechanisms underlying growth ischaemic scenario remain poorly understood. Here, we show that cardiomyocytes subjected ischaemia exosomes elicit angiogenic response endothelial (ECs).Exosomes...
The inflammatory cytokines interleukin-1β and tumor necrosis factor-α (TNF-α) have been identified as mediators of several forms neurodegeneration in the brain. However, they can produce either deleterious or beneficial effects on neuronal function. We investigated these death caused by exposure mouse organotypic hippocampal slice cultures to toxic concentrations AMPA. Either potentiation excitotoxicity neuroprotection was observed, depending concentration timing exposure. A relatively high...
Abstract Methamphetamine (METH) causes irreversible damage to brain cells leading neurological and psychiatric abnormalities. However, the mechanisms underlying life‐threatening effects of acute METH intoxication remain unclear. Indeed, most hypotheses focused on intra‐neuronal events, such as dopamine oxidation, oxidative stress excitotoxicity. Yet, recent reports suggested that glia may contribute METH‐induced neuropathology. In present study, we investigated hippocampal dysfunction...
The mechanisms by which methamphetamine (METH) causes neurotoxicity are not well understood. Recent studies have suggested that METH‐induced neuropathology may result from a multicellular response in glial cells play prominent role, and so it is plausible to suggest cytokines participate the toxic effects of METH. Therefore, present work we evaluated effect an acute administration METH (30 mg/kg single intraperitoneal injection) on interleukin (IL)‐1β, IL‐6, tumor necrosis factor (TNF)‐α...
Given the modulatory role of neuropeptide Y (NPY) in immune system, we investigated effect NPY on production NO and IL-1β microglia. Upon LPS stimulation, treatment inhibited as well expression inducible nitric-oxide synthase (iNOS). Pharmacological studies with a selective Y(1) receptor agonist antagonists for Y(1), Y(2), Y(5) receptors demonstrated that inhibition iNOS was mediated exclusively through activation. Microglial cells stimulated ATP responded massive release IL-1β, measured by...
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)...
Methamphetamine's (METH) neurotoxicity is thought to be in part due its ability induce blood-brain barrier (BBB) dysfunction. Here, we investigated the effect of METH on properties cultured rat primary brain microvascular endothelial cells (BMVECs). Transendothelial flux doubled response METH, irrespective size tracer used. At same time, transendothelial electrical resistance was unchanged as ultrastructural appearance inter-endothelial junctions and distribution key junction proteins,...
It is well known that methamphetamine (METH) neurotoxic and recent studies have suggested the involvement of neuroinflammatory processes in brain dysfunction induced by misuse this drug. Indeed, glial cells seem to be activated response METH, but its effects on microglial are not fully understood. Moreover, it has been shown cytokines, which normally released microglia, may a dual role injury. This led us study toxic effect METH looking cell death alterations tumor necrosis factor-alpha...
Excitation/inhibition (E/I) imbalance remains a widely discussed hypothesis in autism spectrum disorders (ASD). The presence of such an may potentially define therapeutic target for the treatment cognitive disabilities related to this pathology. Consequently, study monogenic autism, as neurofibromatosis type 1 (NF1), represents promising approach isolate mechanisms underlying ASD-related disabilities. However, NF1 mouse model showed increased γ-aminobutyric acid (GABA) neurotransmission,...
Nervous tissue homeostasis requires the regulation of microglia activity. Using conditional gene targeting in mice, we demonstrate that genetic ablation small GTPase Rhoa adult is sufficient to trigger spontaneous activation, producing a neurological phenotype (including synapse and neuron loss, impairment long-term potentiation [LTP], formation β-amyloid plaques, memory deficits). Mechanistically, loss triggers Src activation Src-mediated tumor necrosis factor (TNF) production, leading...
Worldwide, millions of people are exposed to dietary imbalance that impacts in health and quality life. In developing countries, like Brazil, poor settings, habits, traditionally hypoproteic, changing rapidly western-type high-fat foods. These habits imposing new challenges human there many questions the field remain be answered. Accordingly, we currently do not know if chronic consumption hypoproteic (regional basic diet, RBD) or diets (HFD) may impact brain physiology, contributing...
Brain metastasis (BrM) is a devastating end-stage neurological complication that occurs in up to 50% of human epidermal growth factor receptor 2-positive (HER2+) breast cancer (BC) patients. Understanding how disseminating tumor cells manage cross the blood-brain barrier (BBB) essential for developing effective preventive strategies. We identified ecto-nucleotidase ENPP1 (ectonucleotide pyrophosphatase/phosphodiesterase 1) as specifically enriched secretome HER2+ brain metastatic cells,...
Increasing evidences suggest that neuropeptide Y (NPY) may act as a key modulator of the cross-talk between brain and immune system in health disease. In present study, we dissected possible inhibitory role NPY upon inflammation-associated microglial cell motility. NPY, through activation Y(1) receptors, was found to inhibit lipopolysaccharide (LPS)-induced microglia (N9 line) Moreover, stimulation with LPS inhibited by IL-1 receptor antagonist (IL-1ra), suggesting involvement endogenous...
Amphetamines exert their persistent addictive effects by activating brain's reward pathways, perhaps through the release of dopamine in nucleus accumbens (and/or other places). On hand, there is a relationship between and all behavioural aspects that involve motor activity it has been demonstrated exercise leads to an increase synthesis dopamine, stimulates neuroplasticity promotes feelings well-being. Moreover, drugs abuse activate overlapping neural systems. Thus, our aim was study...
Glutamate and NPY have been implicated in hippocampal neuropathology temporal lobe epilepsy. Thus, we investigated the involvement of receptors mediating neuroprotection against excitotoxic insults organotypic cultures rat slices. Exposure slice to 2 microM AMPA (alpha-amino-3-hydroxy-5-methyl-isoxazole-4-propionate) induced neuronal degeneration, monitored by propidium iodide uptake, granule cells CA1 pyramidal cells. For dentate cells, selective activation Y1, Y2, or Y5 with 1...
Abstract Glioblastoma multiforme (GBM) is the most common and aggressive primary brain tumor, with an average life expectancy of 12–15 months. GBM highly infiltrated by microglial cells (MG) promoting tumor growth invasiveness. Moreover, microglia activation subsequent neuroinflammation seem to be involved in blood–brain barrier (BBB) dysfunction commonly observed several central nervous system diseases, including tumors. Nevertheless, how crosstalk between interferes BBB function far from...