AI Article Synopsis

  • Hyperammonemia in neonates and infants can disrupt brain development and lead to long-term cognitive issues.
  • Exposure to ammonium affects early axonal growth and alters protein localization in brain cells, but these effects are limited to the initial maturation phase.
  • Creatine supplementation can help protect axons from ammonium toxicity, though it doesn't fully restore energy levels, and this protective effect relies on glial cells.

Article Abstract

Hyperammonemia in neonates and infants affects brain development and causes mental retardation. We report that ammonium impaired cholinergic axonal growth and altered localization and phosphorylation of intermediate neurofilament protein in rat reaggregated brain cell primary cultures. This effect was restricted to the phase of early maturation but did not occur after synaptogenesis. Exposure to NH4Cl decreased intracellular creatine, phosphocreatine, and ADP. We demonstrate that creatine cotreatment protected axons from ammonium toxic effects, although this did not restore high-energy phosphates. The protection by creatine was glial cell-dependent. Our findings suggest that the means to efficiently sustain CNS creatine concentration in hyperammonemic neonates and infants should be assessed to prevent impairment of axonogenesis and irreversible brain damage.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6757846PMC
http://dx.doi.org/10.1523/JNEUROSCI.22-22-09810.2002DOI Listing

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