Sara Pinto

ORCID: 0000-0002-9785-8956
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About
Contact & Profiles
Research Areas
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Amyotrophic Lateral Sclerosis Research
  • Alzheimer's disease research and treatments
  • Extracellular vesicles in disease
  • Neuroscience and Neuropharmacology Research
  • MicroRNA in disease regulation
  • Neuroscience and Neural Engineering
  • Vitamin C and Antioxidants Research
  • Mitochondrial Function and Pathology
  • Vitamin D Research Studies
  • Tryptophan and brain disorders
  • Neurological disorders and treatments
  • Neuroscience of respiration and sleep
  • Cannabis and Cannabinoid Research
  • Neurogenesis and neuroplasticity mechanisms
  • Transcranial Magnetic Stimulation Studies
  • Eicosanoids and Hypertension Pharmacology
  • RNA Research and Splicing
  • Vitamin K Research Studies

University of Lisbon
2017-2024

Instituto de Medicina Molecular João Lobo Antunes
2021

Amyotrophic lateral sclerosis (ALS) is a fatal adult-onset neurodegenerative disorder affecting motor neurons (MNs). Evidences indicate that ALS non-cell autonomous disease in which glial cells participate both onset and progression. Exosomal transfer of mutant copper-zinc superoxide dismutase 1 (mSOD1) from cell-to-cell was suggested to contribute dissemination. Data our group others showed exosomes activated contain inflammatory-related microRNAs (inflamma-miRNAs) recapitulate the donor...

10.3389/fnins.2017.00273 article EN cc-by Frontiers in Neuroscience 2017-05-16

Accumulation of mutated superoxide dismutase 1 (mSOD1) in amyotrophic lateral sclerosis (ALS) involves injury to motor neurons (MNs), activation glial cells and immune unbalance. However, neuroinflammation, besides its detrimental effects, also plays beneficial roles ALS pathophysiology. Therefore, the targeting microglia modulate release inflammatory neurotoxic mediators their exosomal dissemination, while strengthening cell neuroprotective properties, has gained growing interest. We used...

10.3389/fncel.2019.00109 article EN cc-by Frontiers in Cellular Neuroscience 2019-04-09

Alzheimer’s disease (AD) is a neurodegenerative disorder associated with neuron–glia dysfunction and dysregulated miRNAs. We previously reported upregulated miR-124/miR-21 in AD neurons their exosomes. However, glial distribution, phenotypic alterations exosomal spread are scarcely documented. Here, we show cell activation miR-21 overexpression mouse organotypic hippocampal slices transplanted SH-SY5Y cells expressing the human APP695 Swedish mutation. The upregulation of only CSF from small...

10.3390/cells11213377 article EN cc-by Cells 2022-10-26

Neuronal miRNA dysregulation may have a role in the pathophysiology of Alzheimer’s disease (AD). miRNA(miR)-124 is largely abundant and critical player many neuronal functions. However, lack models reliably recapitulating AD hampers our understanding miR-124’s disease. Using classical human SH-SY5Y-APP695 Swedish neuroblastoma cells (SH-SWE) PSEN1 mutant iPSC-derived neurons (iNEU-PSEN), we observed sustained upregulation miR-124/miR-125b/miR-21, but only miR-124 was consistently shuttled...

10.3390/cells10092424 article EN cc-by Cells 2021-09-14

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease, involving the selective degeneration of cortical upper synapses in primary motor cortex (M1). Excitotoxicity ALS occurs due to an imbalance between excitation and inhibition, closely linked loss/gain astrocytic function. Using SOD1

10.1016/j.nbd.2024.106435 article EN cc-by Neurobiology of Disease 2024-02-07

Abstract The medial prefrontal cortex (mPFC) is involved in cognitive functions such as working memory. Astrocytic cannabinoid type 1 receptor (CB1R) induces cytosolic calcium (Ca 2+ ) concentration changes with an impact on neuronal function. mPFC astrocytes also express adenosine A and 2A receptors (A R, R), being unknown the crosstalk between CB1R these cells. We show here that a further level of regulation astrocyte Ca signaling occurs through CB1R‐A R or heteromers ultimately synaptic...

10.1002/glia.24518 article EN cc-by-nc-nd Glia 2024-03-14

Abstract Alzheimer’s Disease (AD) is characterized by progressive cognitive decline and synaptic dysfunction, often associated with amyloid-beta accumulation microglial alterations. Here, we investigate the role of Sodium-dependent Vitamin C Transporter 2 (SVCT2) in microglia to modulate AD-like pathology mice. Using a combination RNA sequencing, advanced quantitative proteomics, electrophysiology, behavioral tests, high-throughput imaging, viral gene delivery, explore interplay between...

10.1101/2024.02.29.582679 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2024-03-04

Abstract It is known that astrocytes, by the Ca 2+ -dependent release of gliotransmitters, which then act in pre- and post-synaptic receptors, modulate neuronal transmission plasticity. Thus, hippocampal θ-burst long-term potentiation (LTP), a form synaptic plasticity, can be modulated since these cells gliotransmitters are crucial for maintenance LTP. Therefore, this study, we hypothesized facilitatory action BDNF upon LTP would involve astrocytes. To address possibility, fEPSP recordings...

10.1101/2021.03.30.437538 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2021-03-30

Event Abstract Back to A1 polarized IPSCs-derived astrocytes with the PSEN1EΔ9 mutation show deregulated inflammatory dynamics Sofia Ferreira1, Gonçalo F. Garcia1, Sara Pinto1, Filipa Moreira1, Minna Oksanen2, Jari Koistinaho2, Adelaide Fernandes1, 3 and Dora Brites1, 3* 1 Research Institute for Medicines (iMed.ULisboa), Portugal 2 A.I. Virtanen Molecular Sciences, Faculty of Health University Eastern Finland, Finland Faculdade de Farmácia, Universidade Lisboa, Department Biochemistry Human...

10.3389/conf.fncel.2019.01.00025 article EN cc-by Frontiers in Cellular Neuroscience 2019-01-01
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