ArticleScientific reports2017
Thiamine metabolism is critical for regulating correlated growth of dendrite arbors and neuronal somata.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 20 citations in OpenAlex.
- Hippocampal, Microglial, Morphological, and Amyloid Profiles Following Thiamine Pyrophosphate Treatment in 3xTg-AD Mice.International journal of molecular sciences · 2026Article
- Investigation into the Anti-hyperglycemic Traits and Bioactive Constituents of Postbiotics Derived from Lacticaseibacillus paracasei NCUH012072.Probiotics and antimicrobial proteins · 2026Article
- SLC25A19 drives colorectal cancer progression by regulating p53.Cancer medicine · 2024Article
- Alzheimer's disease is associated with disruption in thiamin transport physiology: A potential role for neuroinflammation.Neurobiology of disease · 2022Article
- Reduced Midbrain Dopamine Neuron Number in the Adult Non-human Primate Brain after Fetal Radiation Exposure.Neuroscience · 2020Article
- Genome-Wide Epistatic Interaction Networks Affecting Feed Efficiency in Duroc and Landrace Pigs.Frontiers in genetics · 2020Article
- Rac1 Modulates Excitatory Synaptic Transmission in Mouse Retinal Ganglion Cells.Neuroscience bulletin · 2019Article
- Neurological, Psychiatric, and Biochemical Aspects of Thiamine Deficiency in Children and Adults.Frontiers in psychiatry · 2019Review
- Computing neurite outgrowth and arborization in superior cervical ganglion neurons.Brain research bulletin · 2019Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Thiamine is critical for cellular function, as its phosphorylated and active form, thiamine diphosphate (TDP), acts as coenzyme for three key enzymes in glucose metabolism. Mutations in thiamine transporter, TDP synthesizing enzyme or carrier, including solute carrier family 19 member 3 (SLC19A3), thiamine pyrophosphokinase (TPK1) and solute carrier family 25 member 19 (SLC25A19), have been associated with developmental neurological disorders, including microcephaly and Leigh syndrome. However, little is known about how thiamine metabolism regulates neuronal morphology at the cellular level. Here, using primary rat hippocampal neuronal cultures, we showed that reducing the expression of Tpk1, Slc25a19 or Slc19a3 in individual neurons significantly reduced dendrite complexity, as measured by total dendritic branch tip number (TDBTN) and total dendritic branch length (TDBL). The specificity of the RNAi effects were verified by overexpression of RNAi resistant human constructs. Importantly, changes in both TDBTN and TDBL tightly correlated with reduction in soma size, demonstrating coordinated regulation of soma and dendrite growth by thiamine. The requirement of thiamine metabolism for coordinated somata and dendrite growth is highly consistent with the microcephaly and neurodegenerative phenotypes observed in thiamine loss-of-function diseases.
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