Evidence map›Paper›PMID 31308796›Full record

ArticleExperimental neurobiology2019

Quantitative Proteomic Analysis Reveals Impaired Axonal Guidance Signaling in Human Postmortem Brain Tissues of Chronic Traumatic Encephalopathy.

Baibin Bi, Han-Pil Choi, Seung Jae Hyeon, Shengnan Sun, Ning Su, Yuguang Liu, Junghee Lee, Neil W Kowall, Ann C McKee, Jing-Hua Yang and 1 more

Open access · diamondAbstract read
In one paragraph

Article in Experimental neurobiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
0.8field-weighted citation impact, top 27% 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

14 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.

  1. Pooled it
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  9. Acute Treatment with the M-Channel (KNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023
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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

11 authors at 6 institutions in 3 countries.

Baibin BiDepartments of Neurology, Pathology, and Surgery, Boston University School of Medicine, Boston, MA 02118, USA.
Han-Pil ChoiProteomics Laboratory, VA Boston Healthcare System, Boston, MA 02130, USA.
Seung Jae HyeonCenter for Neuromedicine, Brain Science Institute, Korea Institute of Science and Technology, Seoul 04535, Korea.
Shengnan SunCancer Research Center, Shandong University School of Medicine, Jinan 250012, China.
Ning SuDepartments of Neurology, Pathology, and Surgery, Boston University School of Medicine, Boston, MA 02118, USA.
Yuguang LiuDepartment of Neurosurgery, Qilu Hospital of Shandong University, Jinan 250012, China.
Junghee LeeDepartments of Neurology, Pathology, and Surgery, Boston University School of Medicine, Boston, MA 02118, USA.
Neil W KowallDepartments of Neurology, Pathology, and Surgery, Boston University School of Medicine, Boston, MA 02118, USA.
Ann C McKeeDepartments of Neurology, Pathology, and Surgery, Boston University School of Medicine, Boston, MA 02118, USA.
Jing-Hua YangDepartments of Neurology, Pathology, and Surgery, Boston University School of Medicine, Boston, MA 02118, USA.
Hoon RyuDepartments of Neurology, Pathology, and Surgery, Boston University School of Medicine, Boston, MA 02118, USA.
Boston University · USVA Boston Healthcare System · USShandong University · CNKorea Institute of Brain Science · KRKorea Institute of Science and Technology · KRQilu Hospital of Shandong University · CN

Funding

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
NINDS NIH HHS R01 NS067283NINDS NIH HHS U01 NS086659
6 · The paper itself

Abstract

Chronic traumatic encephalopathy (CTE) is a distinct neurodegenerative disease that associated with repetitive head trauma. CTE is neuropathologically defined by the perivascular accumulation of abnormally phosphorylated tau protein in the depths of the sulci in the cerebral cortices. In advanced CTE, hyperphosphorylated tau protein deposits are found in widespread regions of brain, however the mechanisms of the progressive neurodegeneration in CTE are not fully understood. In order to identify which proteomic signatures are associated with CTE, we prepared RIPA-soluble fractions and performed quantitative proteomic analysis of postmortem brain tissue from individuals neuropathologically diagnosed with CTE. We found that axonal guidance signaling pathwayrelated proteins were most significantly decreased in CTE. Immunohistochemistry and Western blot analysis showed that axonal signaling pathway-related proteins were down regulated in neurons and oligodendrocytes and neuron-specific cytoskeletal proteins such as TUBB3 and CFL1 were reduced in the neuropils and cell body in CTE. Moreover, oligodendrocyte-specific proteins such as MAG and TUBB4 were decreased in the neuropils in both gray matter and white matter in CTE, which correlated with the degree of axonal injury and degeneration. Our findings indicate that deregulation of axonal guidance proteins in neurons and oligodendrocytes is associated with the neuropathology in CTE. Together, altered axonal guidance proteins may be potential pathological markers for CTE.

Indexed as

Axonal guidanceChronic traumatic encephalopathy (CTE)NeurodegenerationNeuronOligodendrocyteQuantitative proteomics

Identifiers

PMID31308796
PMCPMC6614068
OpenAlexW2954418115

What OpenQuestion holds

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LicenceCC BY-NC
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.