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Perinatal asphyxia: CNS development and deficits with delayed onset.

Mario Herrera-Marschitz1, Tanya Neira-Pena2, Edgardo Rojas-Mancilla3

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Frontiers in Neuroscience
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Summary

Perinatal asphyxia can cause long-term neurological deficits. Nicotinamide, a PARP-1 inhibitor, shows promise in preventing these effects by reducing inflammation and protein competition during re-oxygenation.

Keywords:
behaviorcognitiondevelopmentneonatal hypoxic ischemic encephalopathyobstetric complicationsplasticitypoly(ADP-ribose) polymerasesentinel proteins

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Area of Science:

  • Neuroscience
  • Obstetrics
  • Biochemistry

Background:

  • Perinatal asphyxia, a delay or interruption in oxygenation, causes primary and secondary insults.
  • It leads to long-term neurological deficits with unclear mechanisms.
  • Overexpression of poly(ADP-ribose) polymerase-1 (PARP-1) during re-oxygenation is implicated in these deficits.

Purpose of the Study:

  • To investigate the therapeutic potential of nicotinamide, a PARP-1 inhibitor, in mitigating the long-term consequences of perinatal asphyxia.
  • To explore the role of PARP-1 inhibition in preventing neuroinflammation and associated deficits.

Main Methods:

  • An experimental model of global hypoxia was induced in rat fetuses.
  • Following asphyxia, pups were treated with nicotinamide.
  • Nicotinamide's distribution into the brain and its effect on PARP-1 activity were assessed.

Main Results:

  • Nicotinamide rapidly distributed into the brain and inhibited PARP-1 activity.
  • Treatment with nicotinamide prevented several long-term consequences of perinatal asphyxia.
  • Nicotinamide administration down-regulated the expression of pro-inflammatory cytokines.

Conclusions:

  • Nicotinamide is a potential therapeutic agent for perinatal asphyxia.
  • Inhibiting PARP-1 activity is a viable strategy to prevent long-term neurological damage.
  • Nicotinamide serves as a lead compound for developing novel treatments for asphyxia-related complications.