Evidence map›Paper›PMID 28524178›Full record

ArticleExperimental & molecular medicine2017

Transcriptome analyses of chronic traumatic encephalopathy show alterations in protein phosphatase expression associated with tauopathy.

Jeong-Sun Seo, Seungbok Lee, Jong-Yeon Shin, Yu Jin Hwang, Hyesun Cho, Seong-Keun Yoo, Yunha Kim, Sungsu Lim, Yun Kyung Kim, Eun Mi Hwang and 14 more

Open access · goldAbstract read
In one paragraph

Article in Experimental & molecular medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 2 pooled it
1.9field-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

32 citing papers in PubMed, 2 syntheses or guidelines pooled it, 57 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Review
  9. Inhibiting 15-PGDH blocks blood-brain barrier deterioration and protects mice from Alzheimer's disease and traumatic brain injury.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  10. Review
  11. Article
  12. Review
  13. Review
  14. Lipocalin-2 Is a Key Regulator of Neuroinflammation in Secondary Traumatic and Ischemic Brain Injury.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
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

24 authors at 4 institutions in 2 countries.

Jeong-Sun SeoGenomic Medicine Institute (GMI), Medical Research Center, Seoul National University, Seoul, Korea.
Seungbok LeeGenomic Medicine Institute (GMI), Medical Research Center, Seoul National University, Seoul, Korea.
Jong-Yeon ShinGenomic Medicine Institute (GMI), Medical Research Center, Seoul National University, Seoul, Korea.
Yu Jin HwangCenter for Neuromedicine, Brain Science Institute, Korea Institute of Science and Technology, Seoul, Korea.
Hyesun ChoGenomic Medicine Institute (GMI), Medical Research Center, Seoul National University, Seoul, Korea.
Seong-Keun YooGenomic Medicine Institute (GMI), Medical Research Center, Seoul National University, Seoul, Korea.
Yunha KimCenter for Neuromedicine, Brain Science Institute, Korea Institute of Science and Technology, Seoul, Korea.
Sungsu LimCenter for Neuromedicine, Brain Science Institute, Korea Institute of Science and Technology, Seoul, Korea.
Yun Kyung KimCenter for Neuromedicine, Brain Science Institute, Korea Institute of Science and Technology, Seoul, Korea.
Eun Mi HwangCenter for Functional Connectomics, Brain Science Institute, Korea Institute of Science and Technology, Seoul, Korea.
Su Hyun KimCenter for Neuroscience, Brain Science Institute, Korea Institute of Science and Technology, Seoul, Korea.
Chong-Hyun KimCenter for Neuroscience, Brain Science Institute, Korea Institute of Science and Technology, Seoul, Korea.
Seung Jae HyeonCenter for Neuromedicine, Brain Science Institute, Korea Institute of Science and Technology, Seoul, Korea.
Ji-Young YunGenomic Medicine Institute (GMI), Medical Research Center, Seoul National University, Seoul, Korea.
Jihye KimGenomic Medicine Institute (GMI), Medical Research Center, Seoul National University, Seoul, Korea.
Yona KimDepartment of Neurosurgery, Cancer Research Institute, Seoul National University, College of Medicine, Seoul, Korea.
Victor E AlvarezCenter for the Study of Traumatic Encephalopathy, Boston University School of Medicine, Boston, MA, USA.
Thor D SteinCenter for the Study of Traumatic Encephalopathy, Boston University School of Medicine, Boston, MA, USA.
Junghee LeeVA Boston Healthcare System, Boston, MA, USA.
Dong Jin KimCenter for Neuromedicine, Brain Science Institute, Korea Institute of Science and Technology, Seoul, Korea.
Jong-Il KimGenomic Medicine Institute (GMI), Medical Research Center, Seoul National University, Seoul, Korea.ORCID 0000-0002-7240-3744
Neil W KowallVA Boston Healthcare System, Boston, MA, USA.
Hoon RyuCenter for Neuromedicine, Brain Science Institute, Korea Institute of Science and Technology, Seoul, Korea.
Ann C McKeeCenter for the Study of Traumatic Encephalopathy, Boston University School of Medicine, Boston, MA, USA.
Seoul National University · KRKorea Institute of Brain Science · KRBoston University · USSeoul National University Hospital · KR

Funding

Neuropathology CoreP30AG013846 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI KOWALL, NEIL W. · 1996 to 2020
$29.1M
CTE and Posttraumatic Neurodegeneration: Neuropathology and Ex Vivo ImagingU01NS086659 · NINDS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI MCKEE, ANN C. · 2014 to 2017
$6.1M
Epigenetic Regulation of Heterochromatin Condensation in Huntington's DiseaseR01NS067283 · NINDS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI RYU, HOON · 2011 to 2015
$1.2M
NIA NIH HHS P30 AG013846NINDS NIH HHS R01 NS067283NINDS NIH HHS U01 NS086659
6 · The paper itself

Abstract

Chronic traumatic encephalopathy (CTE) is a progressive neurodegenerative disorder that is associated with repetitive head injury and has distinctive neuropathological features that differentiate this disease from other neurodegenerative diseases. Intraneuronal tau aggregates, although they occur in different patterns, are diagnostic neuropathological features of CTE, but the precise mechanism of tauopathy is not known in CTE. We performed whole RNA sequencing analysis of post-mortem brain tissue from patients with CTE and compared the results to normal controls to determine the transcriptome signature changes associated with CTE. The results showed that the genes related to the MAP kinase and calcium-signaling pathways were significantly downregulated in CTE. The altered expression of protein phosphatases (PPs) in these networks further suggested that the tauopathy observed in CTE involves common pathological mechanisms similar to Alzheimer's disease (AD). Using cell lines and animal models, we also showed that reduced PPP3CA/PP2B phosphatase activity is directly associated with increases in phosphorylated (p)-tau proteins. These findings provide important insights into PP-dependent neurodegeneration and may lead to novel therapeutic approaches to reduce the tauopathy associated with CTE.

Indexed as

Protein Processing, Post-TranslationalTranscriptomeAgedAged, 80 and overAnimalsCalcineurinCalcium SignalingChronic Traumatic EncephalopathyDown-RegulationFemaleHEK293 CellsHumansMaleMAP Kinase Signaling SystemMiceMice, Inbred C57BLCalcineurinPPP3CA protein, humantau Proteins

Identifiers

PMID28524178
PMCPMC5454448
OpenAlexW2616038736

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.