Evidence map›Paper›PMID 28060825›Full record

ArticlePloS one2017

Enhanced Activities of Blood Thiamine Diphosphatase and Monophosphatase in Alzheimer's Disease.

Xiaoli Pan, Shaoming Sang, Guoqiang Fei, Lirong Jin, Huimin Liu, Zhiliang Wang, Hui Wang, Chunjiu Zhong

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

11 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
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  4. Review
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  8. Article
  9. Article
  10. Blood-Based Kinase Assessments in Alzheimer's Disease.Frontiers in aging neuroscience · 2018
    Review
  11. Review
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

8 authors at 4 institutions in 1 country.

Xiaoli PanDepartment of Neurology, Zhongshan Hospital & Shanghai Medical College, Fudan University, Shanghai, China.
Shaoming SangDepartment of Neurology, Zhongshan Hospital & Shanghai Medical College, Fudan University, Shanghai, China.
Guoqiang FeiDepartment of Neurology, Zhongshan Hospital & Shanghai Medical College, Fudan University, Shanghai, China.
Lirong JinDepartment of Neurology, Zhongshan Hospital & Shanghai Medical College, Fudan University, Shanghai, China.
Huimin LiuState Key Laboratory of Medical Neurobiology, Institutes of Brain Science & Collaborative Innovation Center for Brain Science, Fudan University, Shanghai, China.
Zhiliang WangRegional Health Service Center of Xujiahui, Xuhui District, Shanghai, China.
Hui WangRegional Health Service Center of Xujiahui, Xuhui District, Shanghai, China.
Chunjiu ZhongDepartment of Neurology, Zhongshan Hospital & Shanghai Medical College, Fudan University, Shanghai, China.
Shanghai Medical College of Fudan University · CNShanghai Xuhui Central Hospital · CNState Key Laboratory of Medical NeurobiologyZhongshan Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThiamine metabolites and activities of thiamine-dependent enzymes are impaired in Alzheimer's disease (AD).

objectiveTo clarify the mechanism for the reduction of thiamine diphosphate (TDP), an active form of thiamine and critical coenzyme of glucose metabolism, in AD.

methodsForty-five AD patients clinically diagnosed and 38 age- and gender-matched control subjects without dementia were voluntarily recruited. The contents of blood TDP, thiamine monophosphate (TMP), and thiamine, as well as the activities of thiamine diphosphatase (TDPase), thiamine monophosphatase (TMPase), and thiamine pyrophosphokinase (TPK), were assayed by high performance liquid chromatography.

resultsBlood TDP contents of AD patients were significantly lower than those in control subjects (79.03 ± 23.24 vs. 127.60 ± 22.65 nmol/L, P<0.0001). Activities of TDPase and TMPase were significantly enhanced in AD patients than those in control subjects (TDPase: 1.24 ± 0.08 vs. 1.00 ± 0.04, P < 0.05; TMPase: 1.22 ± 0.04 vs. 1.00 ± 0.06, P < 0.01). TPK activity remained unchanged in AD as compared with that in control (0.93 ± 0.04 vs. 1.00 ± 0.04, P > 0.05). Blood TDP levels correlated negatively with TDPase activities (r = -0.2576, P = 0.0187) and positively with TPK activities (r = 0.2426, P = 0.0271) in all participants.

conclusionEnhanced TDPase and TMPase activities may contribute to the reduction of TDP level in AD patients. The results imply that an imbalance of phosphorylation-dephosphorylation related to thiamine and glucose metabolism may be a potential target for AD prevention and therapy.

Indexed as

Acid Anhydride HydrolasesAgedAged, 80 and overAllelesAlzheimer DiseaseApolipoproteins EBiomarkersBlood GlucoseCase-Control StudiesChromatography, High Pressure LiquidFastingFemaleGenotypeHumansMaleMiddle AgedAcid Anhydride HydrolasesApolipoproteins EBiomarkersBlood Glucosenucleoside-diphosphatasePhosphoric Monoester HydrolasesThiaminethiamine monophosphataseThiamine MonophosphateThiamin Pyrophosphokinase

Identifiers

PMID28060825
PMCPMC5218390
OpenAlexW2568263457

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Registered trials

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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.