Evidence map›Paper›PMID 31727875›Full record

ArticleExperimental & molecular medicine2019

Deep proteome profiling of the hippocampus in the 5XFAD mouse model reveals biological process alterations and a novel biomarker of Alzheimer's disease.

Dong Kyu Kim, Dohyun Han, Joonho Park, Hyunjung Choi, Jong-Chan Park, Moon-Yong Cha, Jongmin Woo, Min Soo Byun, Dong Young Lee, Youngsoo Kim and 1 more

Open access · goldAbstract read
In one paragraph

Article in Experimental & molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed, 1 pooled it
5.0field-weighted citation impact, top 4% 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

44 citing papers in PubMed, 1 synthesis or guideline pooled it, 89 citations in OpenAlex.

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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 2 institutions in 2 countries.

Dong Kyu Kim *Department of Biomedical Sciences, Seoul National University, College of Medicine, Seoul, Korea.
Dohyun Han *Proteomics Core Facility, Transdisciplinary Research and Collaboration, Biomedical Research Institute, Seoul National University Hospital, Seoul, Korea.ORCID http://orcid.org/0000-0002-0841-1598
Joonho ParkInterdisciplinary Program for Bioengineering, Seoul National University, College of Engineering, Seoul, Korea.
Hyunjung ChoiInterdisciplinary Graduate Program in Genetic Engineering, Seoul National University, Seoul, Korea.
Jong-Chan ParkDepartment of Biomedical Sciences, Seoul National University, College of Medicine, Seoul, Korea.
Moon-Yong ChaLG Chem Life Science R&D Campus, Drug Discovery Center, Seoul, Korea.
Jongmin WooDepartment of Biomedical Sciences, Seoul National University, College of Medicine, Seoul, Korea.
Min Soo ByunInstitute of Human Behavioral Medicine, Medical Research Center, Seoul National University, Seoul, Korea.
Dong Young LeeDepartment of Psychiatry, Seoul National University College of Medicine, Seoul, Republic of Korea.
Youngsoo KimDepartment of Biomedical Sciences, Seoul National University, College of Medicine, Seoul, Korea. biolab@snu.ac.kr.ORCID http://orcid.org/0000-0001-8881-0662
Inhee Mook-JungDepartment of Biomedical Sciences, Seoul National University, College of Medicine, Seoul, Korea. inhee@snu.ac.kr.
Seoul National University · KRSeoul National University Hospital · KR

Funding

National Research Foundation of Korea (NRF) 2014M3C7A1046042National Research Foundation of Korea (NRF) 2014M3C7A1046047National Research Foundation of Korea (NRF) 2015M3C7A1028790National Research Foundation of Korea (NRF) 2017M3C9A5031597National Research Foundation of Korea (NRF) 2018R1A2A1A19019062National Research Foundation of Korea (NRF) 2018R1A5A2025964
6 · The paper itself

Abstract

Alzheimer's disease (AD), which is the most common type of dementia, is characterized by the deposition of extracellular amyloid plaques. To understand the pathophysiology of the AD brain, the assessment of global proteomic dynamics is required. Since the hippocampus is a major region affected in the AD brain, we performed hippocampal analysis and identified proteins that are differentially expressed between wild-type and 5XFAD model mice via LC-MS methods. To reveal the relationship between proteomic changes and the progression of amyloid plaque deposition in the hippocampus, we analyzed the hippocampal proteome at two ages (5 and 10 months). We identified 9,313 total proteins and 1411 differentially expressed proteins (DEPs) in 5- and 10-month-old wild-type and 5XFAD mice. We designated a group of proteins showing the same pattern of changes as amyloid beta (Aβ) as the Aβ-responsive proteome. In addition, we examined potential biomarkers by investigating secretory proteins from the Aβ-responsive proteome. Consequently, we identified vitamin K-dependent protein S (PROS1) as a novel microglia-derived biomarker candidate in the hippocampus of 5XFAD mice. Moreover, we confirmed that the PROS1 level in the serum of 5XFAD mice increases as the disease progresses. An increase in PROS1 is also observed in the sera of AD patients and shows a close correlation with AD neuroimaging markers in humans. Therefore, our quantitative proteome data obtained from 5XFAD model mice successfully predicted AD-related biological alterations and suggested a novel protein biomarker for AD.

Indexed as

Alzheimer DiseaseAnimalsBiomarkersCalcium-Binding ProteinsCells, CulturedChromatography, LiquidFemaleHippocampusHumansMass SpectrometryMiceMice, TransgenicMicrogliaProteomeProteomicsBiomarkersCalcium-Binding ProteinsPros1 protein, mouseProteome

Identifiers

PMID31727875
PMCPMC6856180
OpenAlexW2986407147

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.