María Sancho‐Alonso

ORCID: 0000-0002-6469-5441
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About
Contact & Profiles
Research Areas
  • Neuroscience and Neuropharmacology Research
  • Mitochondrial Function and Pathology
  • Tryptophan and brain disorders
  • Infectious Encephalopathies and Encephalitis
  • Parkinson's Disease Mechanisms and Treatments
  • Stress Responses and Cortisol
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Liver Disease Diagnosis and Treatment
  • Diet and metabolism studies
  • Neurological disorders and treatments
  • Pharmacological Effects and Toxicity Studies
  • Endoplasmic Reticulum Stress and Disease
  • Phosphodiesterase function and regulation
  • Gastrointestinal motility and disorders
  • Metabolism and Genetic Disorders
  • Drug Transport and Resistance Mechanisms
  • Sphingolipid Metabolism and Signaling

Centro de Investigación Biomédica en Red de Salud Mental
2023-2025

Institut d'Investigacions Biomèdiques de Barcelona
2023-2025

Instituto de Salud Carlos III
2023-2025

Centro de Investigacion Principe Felipe
2019-2024

Consorci Institut D'Investigacions Biomediques August Pi I Sunyer
2023-2024

Consejo Superior de Investigaciones Científicas
2023-2024

Universitat de València
2024

Enhanced GABAergic neurotransmission contributes to impairment of motor coordination and gait cognitive function in different pathologies, including hyperammonemia hepatic encephalopathy. Neuroinflammation is a main contributor enhancement through increased activation pathways. For example, enhanced the TNFα–TNFR1-NF-κB-glutaminase-GAT3 pathway TNFα-TNFR1-S1PR2-CCL2-BDNF-TrkB cerebellum hyperammonemic rats enhances neurotransmission. This mediated by mechanisms affecting GABA synthesizing...

10.3389/fphar.2024.1358323 article EN cc-by Frontiers in Pharmacology 2024-03-15

Activated microglia and increased brain IL-1β play a main role in cognitive impairment much pathology. We studied the of neuroinflammation-induced following different types learning memory: novel object recognition (NOR), location (NOL), spatial learning, reference memory (RM), working (WM). All these processes are impaired hyperammonemic rats. assessed which restored by blocking IL-1 receptor vivo rats possible mechanisms involved. Blocking reversed microglial activation hippocampus,...

10.1096/fj.201900230rr article EN The FASEB Journal 2019-06-04

Hyperammonemia contributes to hepatic encephalopathy. In hyperammonemic rats, cognitive function is impaired by altered glutamatergic neurotransmission induced neuroinflammation. The underlying mechanisms remain unclear. Enhanced sphingosine-1-phosphate receptor 2 (S1PR2) activation in the cerebellum of rats we assessed if blocking S1PR2 reduced hippocampal neuroinflammation and reversed impairment signaling pathways were involved. was blocked with intracerebral JTE-013, evaluated. inducing...

10.3390/ijms242417251 article EN International Journal of Molecular Sciences 2023-12-08
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