Evidence map›Paper›PMID 30231926›Full record

ArticleBiological research2018

Thiamine deficiency contributes to synapse and neural circuit defects.

Qiujian Yu, Huimin Liu, Shaoming Sang, Lulan Chen, Yingya Zhao, Yun Wang, Chunjiu Zhong

Open access · goldAbstract read
In one paragraph

Article in Biological research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.7field-weighted citation impact, top 16% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

15 citing papers in PubMed, 27 citations in OpenAlex.

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  14. Thiamine deficiency affects glucose transport and β-oxidation in rats.Journal of animal physiology and animal nutrition · 2019
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Qiujian YuDepartment of Neurology, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
Huimin LiuDepartment of Neurology, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
Shaoming SangDepartment of Neurology, Zhongshan Hospital, Fudan University, Shanghai, 200032, China. sangshaoming6202@126.com.ORCID http://orcid.org/0000-0001-9803-6930
Lulan ChenInstitutes of Brain Science & Collaborative Innovation Center for Brain Science, State Key Laboratory of Medical Neurobiology, Fudan University, Shanghai, 200032, China.
Yingya ZhaoInstitutes of Brain Science & Collaborative Innovation Center for Brain Science, State Key Laboratory of Medical Neurobiology, Fudan University, Shanghai, 200032, China.
Yun WangInstitutes of Brain Science & Collaborative Innovation Center for Brain Science, State Key Laboratory of Medical Neurobiology, Fudan University, Shanghai, 200032, China.
Chunjiu ZhongDepartment of Neurology, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
Sun Yat-sen University · CNFudan University · CN

Funding

National Key Research and Development Program Foundation of China 2016YFC1306403the National Natural Science Foundation of China 91332201the Natural Science Foundation of Shanghai 13JC1401501
6 · The paper itself

Abstract

backgroundThe 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.

resultsTo 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, Aβ induced spines density decrease was considerably ameliorated.

conclusionsThese 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.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsBlotting, WesternDendritic SpinesDiphosphotransferasesGlucoseHippocampusMaleMice, Inbred C57BLNeuronsRandom AllocationRats, Sprague-DawleyReal-Time Polymerase Chain ReactionSynapsesSynaptic TransmissionAmyloid beta-PeptidesDiphosphotransferasesGlucoseThiamine PyrophosphateAlzheimer’s diseaseAmyloid-βSynaptic dysfunctionThiamine deficiency

Identifiers

PMID30231926
PMCPMC6145320
OpenAlexW2890713750

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.