ArticleScientific reports2021
A new rat model of creatine transporter deficiency reveals behavioral disorder and altered brain metabolism.
Article in Scientific reports, 2021. 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, 32 citations in OpenAlex.
- [Scientific reports · 2025Article
- Creatine transporter (SLC6A8) knockout mice exhibit reduced muscle performance, disrupted mitochondrial CaCell death & disease · 2025Article
- Heterozygous females from a rat model for creatine transporter deficiency reveal altered behavioral response to stressors, normal body weight and slight metabolic changes.Frontiers in neuroscience · 2025Article
- Rescue of myocytes and locomotion throughMolecular therapy. Methods & clinical development · 2024Article
- Probing binding and occlusion of substrate in the human creatine transporter-1 by computation and mutagenesis.Protein science : a publication of the Protein Society · 2024Article
- Article
- Article
- Cell-specific vulnerability to metabolic failure: the crucial role of parvalbumin expressing neurons in creatine transporter deficiency.Acta neuropathologica communications · 2023Article
- Taurine and Creatine Transporters as Potential Drug Targets in Cancer Therapy.International journal of molecular sciences · 2023Review
- Creatine transporter-deficient rat model shows motor dysfunction, cerebellar alterations, and muscle creatine deficiency without muscle atrophy.Journal of inherited metabolic disease · 2022Article
- Review
- Metabolic Basis of Creatine in Health and Disease: A Bioinformatics-Assisted Review.Nutrients · 2021Review
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Creatine is an organic compound used as fast phosphate energy buffer to recycle ATP, important in tissues with high energy demand such as muscle or brain. Creatine is taken from the diet or endogenously synthetized by the enzymes AGAT and GAMT, and specifically taken up by the transporter SLC6A8. Deficit in the endogenous synthesis or in the transport leads to Cerebral Creatine Deficiency Syndromes (CCDS). CCDS are characterized by brain creatine deficiency, intellectual disability with severe speech delay, behavioral troubles such as attention deficits and/or autistic features, and epilepsy. Among CCDS, the X-linked creatine transporter deficiency (CTD) is the most prevalent with no efficient treatment so far. Different mouse models of CTD were generated by doing long deletions in the Slc6a8 gene showing reduced brain creatine and cognitive deficiencies or impaired motor function. We present a new knock-in (KI) rat model of CTD holding an identical point mutation found in patients with reported lack of transporter activity. KI males showed brain creatine deficiency, increased urinary creatine/creatinine ratio, cognitive deficits and autistic-like traits. The Slc6a8
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