ArticleJournal of inherited metabolic disease2019
Deletion of the creatine transporter gene in neonatal, but not adult, mice leads to cognitive deficits.
Article in Journal of inherited metabolic disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 23 citations in OpenAlex.
- Connectomic and behavioural alterations in creatine transporter deficiency are partially normalized by gene therapy.Brain : a journal of neurology · 2026Article
- Dietary formaldehyde: a silent aggravator of diabetes and cognitive impairments.Nutrition & diabetes · 2025Review
- Rescue of myocytes and locomotion throughMolecular therapy. Methods & clinical development · 2024Article
- A Gad2 specific Slc6a8 deletion recapitulates the contextual and cued freezing deficits seen in Slc6a8Brain research · 2024Article
- Epigenetic alterations in creatine transporter deficiency: a new marker for dodecyl creatine ester therapeutic efficacy monitoring.Frontiers in neuroscience · 2024Article
- Article
- Creatine transporter-deficient rat model shows motor dysfunction, cerebellar alterations, and muscle creatine deficiency without muscle atrophy.Journal of inherited metabolic disease · 2022Article
- Review
- A new rat model of creatine transporter deficiency reveals behavioral disorder and altered brain metabolism.Scientific reports · 2021Article
- The Creatine Transporter Unfolded: A Knotty Premise in the Cerebral Creatine Deficiency Syndrome.Frontiers in synaptic neuroscience · 2020Review
- Deletion of the Creatine Transporter (Slc6a8) in Dopaminergic Neurons Leads to Hyperactivity in Mice.Journal of molecular neuroscience : MN · 2020Article
- Maternal Creatine Supplementation Positively Affects Male Rat Hippocampal Synaptic Plasticity in Adult Offspring.Nutrients · 2019Article
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Authors and funding
6 authors at 1 institution in 2 countries.
Funding
Abstract
Creatine (Cr) is a guanidino compound that provides readily available phosphate pools for the regeneration of spent adenosine triphosphate (ATP). The lack of brain Cr causes moderate to severe intellectual disability, language impairment, and epilepsy. The most prevalent cause of Cr deficiency are mutations in the X-linked SLC6A8 (Creatine transporter; CrT) gene, known as CrT deficiency (CTD). One of the most critical areas that need to be addressed is whether Cr is necessary for brain development. To address this concern, the Slc6a8 gene was knocked out in either neonatal (postnatal day (P)5) or adult (P60) mice using a tamoxifen-inducible Cre recombinase driven by the human ubiquitin C (UBC) promoter. Mice were tested in the Morris water maze, novel, object recognition, and conditioned fear 60 days after Slc6a8 deletion. In addition, overnight locomotor activity was analyzed. Mice that had the gene deleted on P5 showed deficits in the Morris water maze and novel object recognition, while there were no deficits in P60 knockout mice. Interestingly, the P5 knockout mice showed hyperactivity during the dark phase; however, when examining control mice, the effect was due to the administration of tamoxifen from P5 to 10. Taken together, the results of this study show that Cr is necessary during periods of brain development involved in spatial and object learning. This study also highlights the continued importance of using proper control groups for behavioral testing.
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