Evidence map›Paper›PMID 32483284›Full record

ArticleScientific reports2020

Alterations of transcriptome signatures in head trauma-related neurodegenerative disorders.

Hyesun Cho, Seung Jae Hyeon, Jong-Yeon Shin, Victor E Alvarez, Thor D Stein, Junghee Lee, Neil W Kowall, Ann C McKee, Hoon Ryu, Jeong-Sun Seo

Open access · goldAbstract readComparative Study
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 22% 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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.

  1. Systematic review and meta-analysis of bulk RNAseq studies in human Alzheimer's disease brain tissue.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
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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

10 authors at 5 institutions in 3 countries.

Hyesun ChoGong-Wu Genomic Medicine Institute, Seoul National University Bundang Hospital, Seongnam, 13605, Republic of Korea.
Seung Jae HyeonCenter for Neuromedicine, Brain Science Institute, Korea Institute of Science and Technology, Seoul, 02792, Republic of Korea.
Jong-Yeon ShinGenomic Institute, Macrogen Inc., Seoul, 08511, Republic of Korea.
Victor E AlvarezBoston Univeristy Chronic Traumatic Encephalopathy (CTE) Center, Boston University School of Medicine, Boston, MA, 02118, USA.
Thor D SteinBoston Univeristy Chronic Traumatic Encephalopathy (CTE) Center, Boston University School of Medicine, Boston, MA, 02118, USA.ORCID http://orcid.org/0000-0001-6954-4477
Junghee LeeVA Boston Healthcare System, Boston, MA, 02130, USA.
Neil W KowallVA Boston Healthcare System, Boston, MA, 02130, USA.
Ann C McKeeBoston Univeristy Chronic Traumatic Encephalopathy (CTE) Center, Boston University School of Medicine, Boston, MA, 02118, USA. amckee@bu.edu.
Hoon RyuCenter for Neuromedicine, Brain Science Institute, Korea Institute of Science and Technology, Seoul, 02792, Republic of Korea. hoonryu@bu.edu.
Jeong-Sun SeoGong-Wu Genomic Medicine Institute, Seoul National University Bundang Hospital, Seongnam, 13605, Republic of Korea. jeongsun@snu.ac.kr.
Boston University · USKorea Institute of Brain Science · KRMacrogen (South Korea) · KRSeoul National University · KRSeoul National University Bundang 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
Tau Pathology in CTE vs. Alzheimer's Disease: Microvasculopathy and NeuroinflammationRF1AG057902 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI MCKEE, ANN C. · 2017 to 2017
$4.1M
Epigenetic changes in synaptic and inflammatory genes involved in the age-dependent development of Alzheimer's disease pathologies andcognitive declineRF1AG054156 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI AU, RHODA, RYU, HOON · 2016 to 2018
$3.4M
Modulation of neuronal atrophy in Huntington's diseaseR01NS109537 · NINDS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI LEE, JUNGHEE · 2018 to 2022
$1.4M
The neuropathology of mild traumatic brain injury in Alzheimer's diseaseI01CX001038 · VA · EDITH NOURSE ROGERS MEMORIAL VETERANS HOSPITAL · PI STEIN, THOR · 2015 to 2022
–
CSRD VA I01 CX001038NIA NIH HHS P30 AG013846NIA NIH HHS RF1 AG054156NIA NIH HHS RF1 AG057902NINDS NIH HHS R01 NS109537NINDS NIH HHS U01 NS086659
6 · The paper itself

Abstract

Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease that is associated with repetitive traumatic brain injury (TBI). CTE is known to share similar neuropathological features with Alzheimer's disease (AD), but little is known about the molecular properties in CTE. To better understand the neuropathological mechanism of TBI-related disorders, we conducted transcriptome sequencing analysis of CTE including AD and CTE with AD (CTE/AD) post-mortem human brain samples. Through weighted gene co-expression network analysis (WGCNA) and principal component analysis (PCA), we characterized common and unique transcriptome signatures among CTE, CTE/AD, and AD. Interestingly, synapse signaling-associated gene signatures (such as synaptotagmins) were commonly down-regulated in CTE, CTE/AD, and AD. Quantitative real-time PCR (qPCR) and Western blot analyses confirmed that the levels of synaptotagmin 1 (SYT1) were markedly decreased in CTE and AD compared to normal. In addition, calcium/calmodulin-dependent protein kinase II (CaMKII), protein kinase A (PKA), protein kinase C (PKC), and AMPA receptor genes that play a pivotal role in memory function, were down-regulated in head trauma-related disorders. On the other hand, up-regulation of cell adhesion molecules (CAMs) associated genes was only found in CTE. Our results indicate that dysregulation of synaptic transmission- and memory function-related genes are closely linked to the pathology of head injury-related disorder and AD. Alteration of CAMs-related genes may be specific pathological markers for the CTE pathology.

Indexed as

TranscriptomeAgedAged, 80 and overAlzheimer DiseaseBlotting, WesternCell Adhesion MoleculesChronic Traumatic EncephalopathyCraniocerebral TraumaEndothelial CellsFemaleGene OntologyGene Regulatory NetworksHumansMaleMemoryMiddle AgedCell Adhesion MoleculesNerve Tissue Proteins

Identifiers

PMID32483284
PMCPMC7264177
OpenAlexW3032131520

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.