Andrés Vicente-Acosta's research while affiliated with Universidad Autónoma de Madrid and other places

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Publications (3)

THE SONIC HEDGEHOG AGONIST SAG ATTENUATES MITOCHONDRIAL DYSFUNCTION AND DECREASES THE NEUROTOXOCITY INDUCED BY FRATAXIN-DEFICIENT ASTROCYTES
Article
  • Jun 2022
Friedreich’s ataxia (FRDA) is predominantly a neurodegenerative disease caused by the deficiency of a protein called frataxin (FXN). Although the main pathological alterations are observed in neurons, it is becoming clear that other non-neuronal cells such as astrocytes may be actively involved in the neurodegenerative process associated with the d...
FIGURE 2 | The ECS functioning in astrocytes. (A). In physiological...
FIGURE 3 | The ECS functioning in oligodendrocytes. (A). Under...
Cannabinoids as Glial Cell Modulators in Ischemic Stroke: Implications for Neuroprotection
Article
Full-text available
  • Jun 2022
Stroke is the second leading cause of death worldwide following coronary heart disease. Despite significant efforts to find effective treatments to reduce neurological damage, many patients suffer from sequelae that impair their quality of life. For this reason, the search for new therapeutic options for the treatment of these patients is a priorit...
In vitro characterization of FXN silencing in HAs.A–C HAs were...
Chronic treatment with SAG improves cell metabolism of FXN-deficient...
SAG positively modifies mitochondrial morphology and dynamics of...
Chronic treatment with SAG improves mitochondrial function and activity...
+3 FXN deficiency induces a reactive phenotype in HAs that is attenuated...
The smoothened agonist SAG reduces mitochondrial dysfunction and neurotoxicity of frataxin-deficient astrocytes
Article
Full-text available
  • Apr 2022
Background Friedreich’s ataxia is a rare hereditary neurodegenerative disease caused by decreased levels of the mitochondrial protein frataxin. Similar to other neurodegenerative pathologies, previous studies suggested that astrocytes might contribute to the progression of the disease. To fully understand the mechanisms underlying neurodegeneration...

Citations

... increased COX2 [41] YG8R mice Increased satellite cell proliferation, astrocytosis and influx of OX42 positive cells in the spinal cord and cerebellum [42] FGKO mice Severe ataxia after frataxin deletion in astrocytes during development [43] Microglial cell lines Increased DNA damage after frataxin knockdown [40] Mouse primary astrocytes Increased ROS production after frataxin knockdown [44] Human astrocytes in vitro Impaired mitochondrial activity and superoxide formation; increased release of inflammatory molecules and toxicity for neurons after frataxin knockdown [45,46] iPSC-derived YG8R astrocytes ...
Reference: Neuroinflammation in Friedreich’s Ataxia