Rui O. Costa

ORCID: 0000-0002-2652-7500
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About
Contact & Profiles
Research Areas
  • Alzheimer's disease research and treatments
  • Endoplasmic Reticulum Stress and Disease
  • Nerve injury and regeneration
  • Autophagy in Disease and Therapy
  • Neurogenesis and neuroplasticity mechanisms
  • Nicotinic Acetylcholine Receptors Study
  • Mitochondrial Function and Pathology
  • Prion Diseases and Protein Misfolding
  • Neuroscience and Neuropharmacology Research
  • Ubiquitin and proteasome pathways
  • RNA Interference and Gene Delivery
  • RNA regulation and disease
  • Signaling Pathways in Disease
  • Pancreatic function and diabetes
  • Retinal Development and Disorders
  • Photoreceptor and optogenetics research
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Neuroscience and Neural Engineering
  • Adipokines, Inflammation, and Metabolic Diseases
  • Mesenchymal stem cell research
  • Genetics and Neurodevelopmental Disorders
  • Epigenetics and DNA Methylation
  • Tryptophan and brain disorders
  • RNA Research and Splicing
  • Silk-based biomaterials and applications

University of Coimbra
2013-2025

Centro de Neurociências e Biologia Celular
2006

RELX Group (United Kingdom)
2005

Alzheimer's disease (AD) is the most common cause of dementia in elderly, affecting several million people worldwide. Pathological changes AD brain include presence amyloid plaques, neurofibrillary tangles, loss neurons and synapses, oxidative damage. These strongly associate with mitochondrial dysfunction stress endoplasmic reticulum (ER). Mitochondrial intimately linked to production reactive oxygen species (ROS) mitochondrial-driven apoptosis, which appear be aggravated patients....

10.1155/2012/735206 article EN cc-by International Journal of Cell Biology 2012-01-01

GABAA receptors (GABAAR) are the major players in fast inhibitory neurotransmission central nervous system (CNS). Regulation of GABAAR trafficking and control their surface expression play important roles modulation strength synaptic inhibition. Different pieces evidence show that alterations distribution dysregulation turnover impair activity synapses. A diminished efficacy affects excitatory/inhibitory balance is a common feature various disorders CNS characterized by an increased...

10.3389/fncel.2019.00077 article EN cc-by Frontiers in Cellular Neuroscience 2019-03-07

Summary Alzheimer’s disease (AD) is a progressive neurodegenerative disorder affecting both the hippocampus and cerebral cortex. Reduced synaptic density that occurs early in process seems to be partially due overactivation of N ‐methyl‐ d ‐aspartate receptors (NMDARs) leading excitotoxicity. Recently, we demonstrated amyloid‐beta oligomers (AβO), species implicated loss during initial stages, induce endoplasmic reticulum (ER) stress cultured neurons. Here, investigated whether AβO trigger...

10.1111/j.1474-9726.2012.00848.x article EN Aging Cell 2012-06-18

Abstract Mesenchymal stem cells (MSCs) have been used for cell-based therapies in regenerative medicine, with increasing importance central and peripheral nervous system repair. However, MSCs grafting present disadvantages, such as, a high number of required transplantation low survival rate when transplanted into the (CNS). In line this, secretome which on its composition wide range molecules (neurotrophins, cytokines) microvesicles, can be solution to surpass these problems. effect axonal...

10.1038/s41598-017-03592-1 article EN cc-by Scientific Reports 2017-06-19

Abstract Brain-derived neurotrophic factor (BDNF) is an important mediator of long-term synaptic potentiation (LTP) in the hippocampus. The local effects BDNF depend on activation translation activity, which requires delivery transcripts to synapse. In this work, we found that neuronal activity regulates dendritic localization RNA-binding protein heterogeneous nuclear ribonucleoprotein K (hnRNP K) cultured rat hippocampal neurons by stimulating BDNF-Trk signaling. Microarray experiments...

10.1523/eneuro.0268-17.2017 article EN cc-by-nc-sa eNeuro 2017-11-01

Abstract Neuronal damage in brain ischemia is characterized by a disassembly of the proteasome and decrease its proteolytic activity. However, to what extent these alterations are coupled neuronal death controversial since inhibitors were shown provide protection different models stroke rodents. This question was addressed present work using cultured rat cerebrocortical neurons subjected transient oxygen- glucose-deprivation (OGD) as model for vitro ischemia. Under latter conditions there...

10.1007/s10495-025-02097-x article EN cc-by APOPTOSIS 2025-03-17

Amyloid-β (Aβ) peptide plays a significant role in the pathogenesis of Alzheimer's disease (AD). Previously we found that Aβ induces both mitochondrial and endoplasmic reticulum (ER) dysfunction leading to apoptosis, now address relevance

10.3233/jad-2010-091369 article EN Journal of Alzheimer s Disease 2010-04-01

Ribosomes and a subset of cellular mRNAs are trafficked into axons developing neurons. The axonal localization translational machinery allows new proteins to be rapidly locally synthesized during growth pathfinding. However, in mature neurons, ribosomes significantly reduced or even absent. mechanism that elicits this removal is currently unknown. Here, we demonstrate synapse formation the trigger for ribosome reduction axons. In vivo analysis shows levels decrease rat brain at developmental...

10.1016/j.celrep.2019.06.080 article EN cc-by-nc-nd Cell Reports 2019-07-01

Abstract Prion disorders are progressive neurodegenerative diseases characterized by extensive neuronal loss and the accumulation of pathogenic form prion protein, designated PrP Sc . Recently, we have shown that 106–126 induces endoplasmic reticulum (ER) stress, leading to mitochondrial cytochrome c release, caspase 3 activation apoptotic death. In order further clarify role mitochondria in ER stress‐mediated pathway triggered peptide, investigated effects on Ntera2 human teratocarcinoma...

10.1111/j.1471-4159.2007.05048.x article EN Journal of Neurochemistry 2007-10-09

In recent years, signaling through ubiquitin has been shown to be of great importance for normal brain development. Indeed, fluctuations in levels and spontaneous mutations (de)ubiquitination enzymes greatly perturb synapse formation neuronal transmission. the brain, expression lysine (K) 48-linked chains is higher at a developmental stage coincident with synaptogenesis. Nevertheless, no studies have so far delved into involvement this type polyubiquitin formation. We recently proposed role...

10.3389/fnmol.2016.00043 article EN cc-by Frontiers in Molecular Neuroscience 2016-06-10

This protocol aims at standardizing the procedure to obtain primary cultures of hippocampal and cerebrocortical neurons for in vitro experiments. Cultures should be prepared from cells isolated during embryonic development when neuronal precursor are not yet fully differentiated. helps increasing quality quantity cells, while offering minimal cell death that often occurs dissociation differentiated neurons. Cells plated under appropriate conditions, either Petri-dishes or multi-well plates,...

10.21769/bioprotoc.2551 article EN BIO-PROTOCOL 2017-01-01

Abstract Brain-derived neurotrophic factor (BDNF) is a key mediator of synaptic plasticity and memory formation in the hippocampus. However, BDNF-induced alterations glutamate receptors coupled to glutamatergic synapses hippocampus have not been elucidated. In this work we investigated putative role GluN2B-containing NMDA induced by BDNF. Stimulation hippocampal synaptoneurosomes with BDNF led significant time-dependent increase surface expression as determined immunocytochemistry...

10.1101/2024.10.21.618702 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2024-10-22

Abstract Neuronal damage in brain ischemia is characterized by a disassembly of the proteasome and decrease its proteolytic activity. However, to what extent these alterations are coupled neuronal death controversial since inhibitors were shown provide protection different models stroke rodents. This question was addressed present work using cultured rat cerebrocortical neurons subjected transient oxygen- glucose-deprivation (OGD) as model for vitro ischemia. Under latter conditions there...

10.1101/2024.05.15.594129 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2024-05-15

One the neuropathological hallmarks of Alzheimer's disease (AD) are presence extracellular senile plaques mainly composed fibrillar amyloid-beta peptide (Abeta). An increasing body evidence supports that endoplasmic reticulum (ER) stress and mitochondrial dysfunction have active roles in neurotoxic mechanisms involved neuronal injury triggered by Abeta. This study was aimed to investigate cross-talk between ER mitochondria death induced To achieve this purpose, a first approach,...

10.1016/j.jalz.2008.05.1011 article EN Alzheimer s & Dementia 2008-07-01
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