Neuroprotective effect of melatonin: a novel therapy against perinatal hypoxia-ischemia

Daniel Alonso-Alconada1, Antonia Alvarez, Olatz Arteaga

  • 1Department of Cell Biology and Histology, School of Medicine and Dentistry, University of the Basque Country, Barrio Sarriena s/n, Leioa 48940, Bizkaia, Spain. daniel.alonsoa@ehu.es.

Insights

Perinatal hypoxia-ischemia (HI) causes significant child mortality. Melatonin shows promise as a neuroprotective agent to reduce brain injury from this condition.

Area of Science:

  • Neuroscience
  • Neonatology
  • Pediatric Neurology

Background:

  • Perinatal hypoxia-ischemia (HI) is a leading cause of mortality and long-term disability in children.
  • Despite advances in neonatology, the incidence of HI remains high, necessitating improved therapeutic strategies.
  • Neurological sequelae of HI require effective neuroprotective interventions to minimize lifelong chronic care needs.

Purpose of the Study:

  • To review recent advances in the therapeutic use of melatonin for perinatal hypoxic-ischemic brain injury.
  • To explore the neuroprotective mechanisms of melatonin in the context of neonatal asphyxia.
  • To assess the potential of melatonin as a feasible treatment for cerebral asphyxia.

Main Methods:

  • Literature review of studies on melatonin's neuroprotective effects.
  • Analysis of research investigating melatonin's role in cell survival and physiological modulation.
  • Synthesis of findings related to melatonin's efficacy against perinatal HI.

Main Results:

  • Melatonin demonstrates potential neuroprotective properties against perinatal HI.
  • The hormone aids cell survival through diverse physiological functions.
  • Evidence supports melatonin's therapeutic interest for brain injury following asphyxia.

Conclusions:

  • Melatonin is a promising therapeutic agent for mitigating neurological damage from perinatal HI.
  • Further research into melatonin's mechanisms is warranted.
  • Melatonin represents a feasible future strategy for managing cerebral asphyxia events.