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Thiamine deficiency contributes to synapse and neural circuit defects
Qiujian Yu1, Huimin Liu1, Shaoming Sang2,3
1Department of Neurology, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
Biological Research
|September 21, 2018
Summary
Thiamine diphosphate reduction in Alzheimer's disease (AD) impairs brain glucose metabolism and synaptic function. Benfotiamine treatment showed potential in ameliorating these effects, offering new therapeutic insights.
Area of Science:
- Neuroscience
- Biochemistry
Background:
- Reduced thiamine diphosphate is specific to Alzheimer's disease (AD).
- This reduction is a causal factor in brain glucose hypometabolism, a neurodegenerative index in AD.
- It correlates with cognitive impairment and may cause synaptic and neural circuit dysfunction.
Purpose of the Study:
- To investigate the role of thiamine deficiency in synaptic dysfunction and AD pathogenesis.
- To demonstrate the link between thiamine diphosphate reduction, glucose hypometabolism, and cognitive decline in AD.
Main Methods:
- Induced thiamine deficiency in vitro and in vivo to model glucose metabolism abnormalities.
- Utilized TPK RNAi to lower thiamine levels and assess effects on neuronal function.
- Administered benfotiamine to evaluate its therapeutic potential against amyloid-beta (Aβ) induced effects.
Main Results:
- Thiamine deficiency led to reduced dendrite spine density.
- Lowered excitatory neurotransmission and impaired hippocampal long-term potentiation were observed.
- Benfotiamine treatment ameliorated amyloid-beta induced decrease in spine density.
Conclusions:
- Thiamine deficiency significantly contributes to synaptic dysfunction in AD pathogenesis.
- These findings provide novel insights into the mechanisms of synaptic and neuronal dysfunction in Alzheimer's disease.
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