Evidence map›Paper›PMID 28696436›Full record

ArticleMolecular psychiatry2018

Reduced TRPC6 mRNA levels in the blood cells of patients with Alzheimer's disease and mild cognitive impairment.

R Lu, J Wang, R Tao, J Wang, T Zhu, W Guo, Y Sun, H Li, Y Gao, W Zhang and 9 more

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular psychiatry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

32 citing papers in PubMed, 62 citations in OpenAlex.

  1. Article
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  16. Review
  17. The China Alzheimer Report 2022.General psychiatry · 2022
    Review
  18. Article
  19. Article
  20. 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

19 authors at 9 institutions in 2 countries.

R LuLaboratory of Neural Signal Transduction, Institute of Neuroscience, Chinese Academy of Sciences, Shanghai, China.
J WangLaboratory of Neural Signal Transduction, Institute of Neuroscience, Chinese Academy of Sciences, Shanghai, China.ORCID 0000-0002-6227-6112
R TaoState Key Laboratory of Cell Biology, CAS Center for Excellence in Molecular Cell Science, Shanghai Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China.
J WangDepartment of Neurology and Center for Clinical Neuroscience, Daping Hospital, Third Military Medical University, Chongqing, China.
T ZhuLaboratory of Neural Signal Transduction, Institute of Neuroscience, Chinese Academy of Sciences, Shanghai, China.
W GuoState Key Laboratory of Cell Biology, CAS Center for Excellence in Molecular Cell Science, Shanghai Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China.
Y SunDepartment of Neurology and Institute of Neurology, Huashan Hospital, Shanghai Medical College, Fudan University, Shanghai, China.
H LiDepartment of Neurology and Institute of Neurology, Huashan Hospital, Shanghai Medical College, Fudan University, Shanghai, China.
Y GaoDepartment of Neurology and Institute of Neurology, Rui Jin Hospital affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
W ZhangDepartment of Geriatrics, Tiantan Hospital, Capital Medical University, Beijing, China.
C J FowlerThe Florey Institute, The University of Melbourne, Melbourne, VIC, Australia.
Q LiThe Florey Institute, The University of Melbourne, Melbourne, VIC, Australia.
S ChenDepartment of Neurology and Institute of Neurology, Rui Jin Hospital affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Z WuDepartment of Neurology and Institute of Neurology, Huashan Hospital, Shanghai Medical College, Fudan University, Shanghai, China.
C L MastersThe Florey Institute, The University of Melbourne, Melbourne, VIC, Australia.
C ZhongDepartment of Neurology, Zhongshan Hospital and Shanghai Medical College, State Key Laboratory of Medical Neurobiology, Institute of Brain Science, Fudan University, Shanghai, China.
N JingState Key Laboratory of Cell Biology, CAS Center for Excellence in Molecular Cell Science, Shanghai Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China.
Y WangDepartment of Neurology and Center for Clinical Neuroscience, Daping Hospital, Third Military Medical University, Chongqing, China.
Y WangLaboratory of Neural Signal Transduction, Institute of Neuroscience, Chinese Academy of Sciences, Shanghai, China.
Army Medical University · CNFudan University · CNThe University of Melbourne · AUChinese Academy of Sciences · CNShanghai Jiao Tong University · CNShanghaiTech University · CNCapital Medical University · CNCenter for Excellence in Molecular Cell Science · CNShanghai Medical College of Fudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transient receptor potential canonical 6 (TRPC6) inhibits β-amyloid (Aβ) production. Hyperforin, the TRPC6 agonist, reduces Aβ levels and improves cognitive performance in Alzheimer's disease (AD) models. However, it's unknown whether TRPC6 expression is changed in AD patients. In this case-control study, we measured TRPC6 expression levels in the peripheral blood cells of four independent AD sets from five hospitals and one mild cognitive impairment (MCI) set from a local community (229 AD, 70 MCI, 40 Parkinson disease and 359 controls from China, total n=698) using quantitative real-time PCR assay. We found a specific reduction of TRPC6 mRNA levels in four AD sets and one MCI set. The median TRPC6 mRNA levels were lower in the following: (1) combined AD patients than in age-matched controls (0.78 vs 1.73, P<0.001); (2) mild-to-moderate AD patients than in age-matched controls (0.81 vs 1.73, P<0.001); and (3) MCI patients than in age-matched controls (0.76 vs 1.72, P<0.001). In the receiver-operating characteristic curve analysis, the area under curve was 0.85 for combined AD, 0.84 for mild-to-moderate AD and 0.79 for MCI. In a subgroup of AD patients with brain Aβ examination, TRPC6 was associated with standardized uptake value ratio of Pittsburgh Compound B (Spearman's r=-0.49, P=0.04) and cerebrospinal fluid Aβ42 (Spearman's r=0.43, P=0.04). The TRPC6 reduction in AD patients was further confirmed in blood RNA samples from The Australian Imaging, Biomarkers and Lifestyle Flagship Study of Aging, in post-mortem brain tissues from The Netherlands Brain Bank and in induced pluripotent stem cells-derived neurons from Chinese donors. We conclude that TRPC6 mRNA levels in the blood cells are specifically reduced in AD and MCI patients, and TRPC6 might be a biomarker for the early diagnosis of AD.

Indexed as

AgedAlzheimer DiseaseAnimalsBiomarkersCase-Control StudiesCognitive DysfunctionFemaleHEK293 CellsHumansJurkat CellsMaleMiceMiddle AgedRNA, Messengertau ProteinsTRPC6 Cation ChannelBiomarkersRNA, Messengertau ProteinsTRPC6 Cation ChannelTRPC6 protein, human

Identifiers

PMID28696436
OpenAlexW2734942459

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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.