Evidence map›Paper›PMID 35885023›Full record

ArticleBiomedicines2022

Non-Targeted Metabolomics Approach Revealed Significant Changes in Metabolic Pathways in Patients with Chronic Traumatic Encephalopathy.

Jinkyung Lee, Suhyun Kim, Yoon Hwan Kim, Uiyeol Park, Junghee Lee, Ann C McKee, Kyoung Heon Kim, Hoon Ryu, Jeongae Lee

Open access · goldAbstract read
In one paragraph

Article in Biomedicines, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.2field-weighted citation impact, top 44% 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

2 citing papers in PubMed, 2 citations in OpenAlex.

  1. Article
  2. 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

9 authors at 3 institutions in 2 countries.

Jinkyung LeeCenter for Advanced Biomolecular Recognition, Korea Institute of Science and Technology (KIST), Seoul 02792, Korea.
Suhyun KimBrain Science Institute, Korea Institute of Science and Technology (KIST), Seoul 02792, Korea.
Yoon Hwan KimCenter for Advanced Biomolecular Recognition, Korea Institute of Science and Technology (KIST), Seoul 02792, Korea.
Uiyeol ParkBrain Science Institute, Korea Institute of Science and Technology (KIST), Seoul 02792, Korea.
Junghee LeeBoston University Alzheimer's Disease Research Center (BUADRC), Department of Neurology, Boston University School of Medicine, Boston, MA 02118, USA.
Ann C McKeeBoston University Alzheimer's Disease Research Center (BUADRC), Department of Neurology, Boston University School of Medicine, Boston, MA 02118, USA.
Kyoung Heon KimDepartment of Biotechnology, Graduate School, Korea University, Seoul 02841, Korea.ORCID 0000-0003-4600-8668
Hoon RyuBrain Science Institute, Korea Institute of Science and Technology (KIST), Seoul 02792, Korea.ORCID 0000-0001-6544-3732
Jeongae LeeCenter for Advanced Biomolecular Recognition, Korea Institute of Science and Technology (KIST), Seoul 02792, Korea.
Boston University · USKorea University · KRKorea Institute of Brain Science · KR

Funding

Modulation of neuronal atrophy in Huntington's diseaseR01NS109537 · NINDS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI LEE, JUNGHEE · 2018 to 2022
$1.4M
NINDS NIH HHS R01 NS109537
6 · The paper itself

Abstract

Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease that is frequently found in athletes and those who have experienced repetitive head traumas. CTE is associated with a variety of neuropathologies, which cause cognitive and behavioral impairments in CTE patients. However, currently, CTE can only be diagnosed after death via brain autopsy, and it is challenging to distinguish it from other neurodegenerative diseases with similar clinical features. To better understand this multifaceted disease and identify metabolic differences in the postmortem brain tissues of CTE patients and control subjects, we performed ultra-high performance liquid chromatography-mass spectrometry (UPLC-MS)-based non-targeted metabolomics. Through multivariate and pathway analysis, we found that the brains of CTE patients had significant changes in the metabolites involved in astrocyte activation, phenylalanine, and tyrosine metabolism. The unique metabolic characteristics of CTE identified in this study were associated with cognitive dysfunction, amyloid-beta deposition, and neuroinflammation. Altogether, this study provided new insights into the pathogenesis of CTE and suggested appealing targets for both diagnosis and treatment for the disease.

Indexed as

astrocyte activationcatecholamineschronic traumatic encephalopathy (CTE)non-targeted metabolomicsphenylalanine metabolismtyrosine metabolism

Identifiers

PMID35885023
PMCPMC9313062
OpenAlexW4285733640

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.