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Thiamine deficiency contributes to synapse and neural circuit defects
Yu, Qiujian; Liu, Huimin; Sang, Shaoming; Chen, Lulan; Zhao, Yingya; Wang, Yun; Zhong, Chunjiu.
  • Yu, Qiujian; Fudan University. Zhongshan Hospital. Department of Neurology. Shanghai. CN
  • Liu, Huimin; Fudan University. Zhongshan Hospital. Department of Neurology. Shanghai. CN
  • Sang, Shaoming; Fudan University. Zhongshan Hospital. Department of Neurology. Shanghai. CN
  • Chen, Lulan; Fudan University. State Key Laboratory of Medical Neurobiology. Institutes of Brain Science & Collaborative Innovation Center for Brain Science. Shanghai. CN
  • Zhao, Yingya; Fudan University. State Key Laboratory of Medical Neurobiology. Institutes of Brain Science & Collaborative Innovation Center for Brain Science. Shanghai. CN
  • Wang, Yun; Fudan University. State Key Laboratory of Medical Neurobiology. Institutes of Brain Science & Collaborative Innovation Center for Brain Science. Shanghai. CN
  • Zhong, Chunjiu; Fudan University. Zhongshan Hospital. Department of Neurology. Shanghai. CN
Biol. Res ; 51: 35, 2018. graf
Article in English | LILACS | ID: biblio-983939
ABSTRACT

BACKGROUND:

The previous studies have demonstrated the reduction of thiamine diphosphate is specific to Alzheimer's disease (AD) and causal factor of brain glucose hypometabolism, which is considered as a neurodegenerative index of AD and closely correlates with the degree of cognitive impairment. The reduction of thiamine diphosphate may contribute to the dysfunction of synapses and neural circuits, finally leading to cognitive decline.

RESULTS:

To demonstrate this hypothesis, we established abnormalities in the glucose metabolism utilizing thiamine deficiency in vitro and in vivo, and we found dramatically reduced dendrite spine density. We further detected lowered excitatory neurotransmission and impaired hippocampal long-term potentiation, which are induced by TPK RNAi in vitro. Importantly, via treatment with benfotiamine, Aß induced spines density decrease was considerably ameliorated.

CONCLUSIONS:

These results revealed that thiamine deficiency contributed to synaptic dysfunction which strongly related to AD pathogenesis. Our results provide new insights into pathogenesis of synaptic and neuronal dysfunction in AD.
Subject(s)


Full text: Available Index: LILACS (Americas) Main subject: Synapses / Thiamine Deficiency / Thiamine Pyrophosphate / Alzheimer Disease / Neurons Limits: Animals Language: English Journal: Biol. Res Journal subject: Biology Year: 2018 Type: Article Affiliation country: China Institution/Affiliation country: Fudan University/CN

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Full text: Available Index: LILACS (Americas) Main subject: Synapses / Thiamine Deficiency / Thiamine Pyrophosphate / Alzheimer Disease / Neurons Limits: Animals Language: English Journal: Biol. Res Journal subject: Biology Year: 2018 Type: Article Affiliation country: China Institution/Affiliation country: Fudan University/CN