Synaptoprotection in perinatal asphyxia: an experimental approach
Perinatal asphyxia (PA) is an obstetric complication occurring when the oxygen supply to the newborn is temporally interrupted. This health problem is associated with high morbimortality in term and preterm neonates. It severely affects the brain structure and function, involving cortical, hippoc...
Guardado en:
| Autores principales: | , , , , |
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| Formato: | Artículo |
| Lenguaje: | Inglés |
| Publicado: |
Frontiers
2020
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| Materias: | |
| Acceso en línea: | https://repositorio.uca.edu.ar/handle/123456789/10801 |
| Aporte de: |
| Sumario: | Perinatal asphyxia (PA) is an obstetric complication occurring when the oxygen supply
to the newborn is temporally interrupted. This health problem is associated with high
morbimortality in term and preterm neonates. It severely affects the brain structure
and function, involving cortical, hippocampal, and striatal loss of neurons. Nearly 25%
of PA survivor newborns develop several neurodevelopmental disabilities. Behavioral
alterations, as well as the morphological and biochemical pathways involved in PA
pathophysiology, have been studied using an animal model that resembles intrauterine
asphyxia. Experimental evidence shows that PA induces synaptic derangement. Then,
synaptic dysfunction embodies a putative target for neuroprotective strategies. Over the
last years, therapeutic hypothermia (TH), the only treatment available, has shown positive
results in the clinic. Several pharmacological agents are being tested in experimental
or clinical trial studies to prevent synaptopathy. Preservation of the synaptic structure
and function, i.e., “synaptoprotection,” makes up a promising challenge for reducing
incidental neurodevelopmental disorders associated with PA. Accordingly, here, we
summarize and review the findings obtained from the referred experimental model and
propose a renewed overview in the field. |
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