Evidence map›Paper›PMID 29338754›Full record

ArticleMolecular neurodegeneration2018

Molecular and functional signatures in a novel Alzheimer's disease mouse model assessed by quantitative proteomics.

Dong Kyu Kim, Joonho Park, Dohyun Han, Jinhee Yang, Ahbin Kim, Jongmin Woo, Youngsoo Kim, Inhee Mook-Jung

Open access · goldAbstract read
In one paragraph

Article in Molecular neurodegeneration, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed, 1 pooled it
5.9field-weighted citation impact, top 3% 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

49 citing papers in PubMed, 1 synthesis or guideline pooled it, 103 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Dual Targeting of Tau Kinases and Autophagy by Abemaciclib Independent of CDK4/6 Inhibition.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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  5. Microglial GM3 accumulation impairs Aβ phagocytic activity and promotes neuroinflammation in Alzheimer's disease.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026
    Article
  6. Article
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  8. Review
  9. Article
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  13. Article
  14. FGFR3 drives Aβ-induced tau uptake.Experimental & molecular medicine · 2024
    Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Examining the Effect ofMolecules (Basel, Switzerland) · 2023
    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

8 authors at 2 institutions in 1 country.

Dong Kyu KimDepartment of Biomedical Sciences, Seoul National University, College of Medicine, 103 Daehak-ro, Seoul, 110-799, South Korea.
Joonho ParkInterdisciplinary Program in Bioengineering, College of Engineering, Seoul National University, 1 Gwanak-ro, Seoul, 151-742, South Korea.
Dohyun HanBiomedical Research Institute, Seoul National University Hospital, 101 Daehak-ro, Seoul, 110-744, South Korea.
Jinhee YangDepartment of Biomedical Sciences, Seoul National University, College of Medicine, 103 Daehak-ro, Seoul, 110-799, South Korea.
Ahbin KimDepartment of Biomedical Sciences, Seoul National University, College of Medicine, 103 Daehak-ro, Seoul, 110-799, South Korea.
Jongmin WooDepartment of Biomedical Sciences, Seoul National University, College of Medicine, 103 Daehak-ro, Seoul, 110-799, South Korea.
Youngsoo KimInterdisciplinary Program in Bioengineering, College of Engineering, Seoul National University, 1 Gwanak-ro, Seoul, 151-742, South Korea. biolab@snu.ac.kr.
Inhee Mook-JungDepartment of Biomedical Sciences, Seoul National University, College of Medicine, 103 Daehak-ro, Seoul, 110-799, South Korea. inhee@snu.ac.kr.
Seoul National University · KRSeoul National University Hospital · KR

Funding

National Research Foundation of Korea 2011-0030738National Research Foundation of Korea 2011-0030740National Research Foundation of Korea 2014M3C7A1046047National Research Foundation of Korea 2015M3C7A1028790National Research Foundation of Korea 2015R1A2A1A05001794National Research Foundation of Korea 2017M3C9A5031597
6 · The paper itself

Abstract

backgroundAlzheimer's disease (AD), the most common neurodegenerative disorder, is characterized by the deposition of extracellular amyloid plaques and intracellular neurofibrillary tangles. To understand the pathological mechanisms underlying AD, developing animal models that completely encompass the main features of AD pathologies is indispensable. Although mouse models that display pathological hallmarks of AD (amyloid plaques, neurofibrillary tangles, or both) have been developed and investigated, a systematic approach for understanding the molecular characteristics of AD mouse models is lacking.

methodsTo elucidate the mechanisms underlying the contribution of amyloid beta (Aβ) and tau in AD pathogenesis, we herein generated a novel animal model of AD, namely the AD-like pathology with amyloid and neurofibrillary tangles (ADLP

resultsThe ADLP

conclusionsOur study is the first to compare and describe the proteomic characteristics in amyloid and neurofibrillary tangle pathologies using isobaric label-based quantitative proteomics. Furthermore, we analyzed the hippocampal proteome of the newly developed ADLP

Indexed as

Alzheimer DiseaseDisease Models, AnimalAmyloid beta-Protein PrecursorAnimalsHippocampusHumansMiceMice, TransgenicMutationPresenilin-1Proteomicstau ProteinsTransgenesAmyloid beta-Protein PrecursorAPP protein, humanMAPT protein, humanPresenilin-1PSEN1 protein, humantau Proteins10-plex tandem mass tagAlzheimer’s diseaseAnimal disease modelAβQuantitative proteomicsTau

Identifiers

PMID29338754
PMCPMC5771139
OpenAlexW2782632913

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.