ArticleActa neuropathologica communications2023
Cell-specific vulnerability to metabolic failure: the crucial role of parvalbumin expressing neurons in creatine transporter deficiency.
Article in Acta neuropathologica communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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8 citing papers in PubMed, 16 citations in OpenAlex.
- Dual platform spatial transcriptomics reveals parvalbumin interneuron subtype vulnerability in mouse models of Alzheimer's disease.Nature communications · 2026Article
- AnnQ: reference-based quantification of cellular abnormality at single-cell resolution.Briefings in bioinformatics · 2026Article
- Connectomic and behavioural alterations in creatine transporter deficiency are partially normalized by gene therapy.Brain : a journal of neurology · 2026Article
- Adaptations of the axon initial segment in fast-spiking interneurons of the human neocortex support low action potential thresholds.PLoS biology · 2025Article
- Translatome of dorsal striatum parvalbumin interneurons revisited: insights across diverse experimental paradigms.Frontiers in cellular neuroscience · 2025Article
- Reovirus infection induces transcriptome-wide unique A-to-I editing changes in the murine fibroblasts.Virus research · 2024Article
- A Gad2 specific Slc6a8 deletion recapitulates the contextual and cued freezing deficits seen in Slc6a8Brain research · 2024Article
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16 authors at 6 institutions in 3 countries.
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Abstract
Mutations in the solute carrier family 6-member 8 (Slc6a8) gene, encoding the protein responsible for cellular creatine (Cr) uptake, cause Creatine Transporter Deficiency (CTD), an X-linked neurometabolic disorder presenting with intellectual disability, autistic-like features, and epilepsy. The pathological determinants of CTD are still poorly understood, hindering the development of therapies. In this study, we generated an extensive transcriptomic profile of CTD showing that Cr deficiency causes perturbations of gene expression in excitatory neurons, inhibitory cells, and oligodendrocytes which result in remodeling of circuit excitability and synaptic wiring. We also identified specific alterations of parvalbumin-expressing (PV
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