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Understanding Creatine for Neurological Health in Babies

Circulating and Cerebral Creatine Levels of the Preterm Infant: Implications for Neurological Development.

Status
Completed
Phases
Unknown
Study type
Observational
Source
ANZCTR
Registry ID
ACTRN12618000871246
Acronym
UNICORN Babies
Enrollment
67
Registered
2018-05-22
Start date
2018-08-13
Completion date
2021-01-15
Last updated
2025-09-08

For informational purposes only — not medical advice. Sourced from public registries and may not reflect the latest updates. Terms

Conditions

None listed

Brief summary

Each year around 10% of all babies born in Australia and New Zealand are preterm. Over half of these babies will have acquired brain injury, increasing their risks of developing life-long conditions, such as cerebral palsy. Creatine and its phosphorylated derivative phosphocreatine (PCr) have long been established as having a critical role in neural development and brain metabolism, with creatine deficiency syndromes leading to significant neurological impairments, including mental retardation, expressive speech and language delay, autistic like behaviour and epilepsy. We have evidence from preclinical animal studies to suggest that preterm babies will be creatine deficient due to an immature renal-hepatic axis and inability to make creatine. Our preliminary data from a 26-week preterm infant shows a dramatic fall in plasma creatine concentration over the first week of life, suggesting this baby was unable to maintain creatine homeostasis. These observations taken together raise questions about whether creatine insufficiency predisposes or compounds neurological deficits in preterm infants? We will utilise non-invasive imaging techniques to measure cerebral creatine levels in preterm infants, to determine any creatine deficiencies in this population. The innovation of this work is that early detection of cerebral creatine deficiency in preterm infants will provide the basis of early intervention with creatine supplementation to avoid cerebral energy deficiency and the ensuing development of poor neurological sequela associated with these deficiencies. If our hypothesis is proven, we stand to revolutinise the nutritional care of preterm infants, directly influence brain function and improve the short and long-term neurological outcomes for these babies.

Interventions

Observations [1] Measurement of creatine and associated metabolites in plasma, urine and nutrition samples, collected from preterm babies across the duration of their stay within the NICU; [2] MRI/MRS scan at term equivalent age; [3] Developmental follow up assessment at three months term corrected age.

Sponsors

Hudson Institute of Medical Research/Monash University
Lead SponsorUniversity

Eligibility

Sex/Gender
All
Age
23 Weeks to 40 Weeks
Healthy volunteers
Yes

Inclusion criteria

1. Singleton babies 2. Provision of Signed and Dated Informed Consent from Parent/Guardian 3. Preterm infants of gestational post maternal age receiving care within the Neonatal Intensive Care Unit at CCDHB, or, healthy term infants at 39-40 weeks gestation from low risk pregnancies delivered at CCDHB.

Exclusion criteria

1. Babies with major congenital, genetic or chromosomal abnormalities known to affect neurodevelopmental outcomes 2. Hypoxic ischaemic encephalopathy 3. Inborn (proven or suspected) errors of metabolism 4. Fetal growth restriction (birth weight <10th percentile on customised percentiles)

Outcome results

None listed

Source: ANZCTR · Data processed: Feb 21, 2026