Evidence map›Paper›PMID 39529733›Full record

ArticleFrontiers in dementia2024

Quantitative proteomic analysis using a mouse model of Lewy body dementia induced by α-synuclein preformed fibrils injection.

Fatih Akkentli, In Kyu Jang, Yoonseop Choi, Young Min, Jinhee Park, Heejin Jo, Leoni Kim, Aashi Mendpara, Bikram Bains, Dongyoon Yoo and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in dementia, 2024. 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
–field-weighted citation impact
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.

  1. Review
  2. Review
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

13 authors.

Fatih Akkentli *Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD, United States.
In Kyu Jang *Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD, United States.
Yoonseop Choi *Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD, United States.
Young MinNeuroregeneration and Stem Cell Programs, Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD, United States.
Jinhee ParkNeuroregeneration and Stem Cell Programs, Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD, United States.
Heejin JoNeuroregeneration and Stem Cell Programs, Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD, United States.
Leoni KimNeuroregeneration and Stem Cell Programs, Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD, United States.
Aashi MendparaNeuroregeneration and Stem Cell Programs, Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD, United States.
Bikram BainsNeuroregeneration and Stem Cell Programs, Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD, United States.
Dongyoon YooNeuroregeneration and Stem Cell Programs, Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD, United States.
Jinchong XuNeuroregeneration and Stem Cell Programs, Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD, United States.
Chan Hyun NaNeuroregeneration and Stem Cell Programs, Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD, United States.
Sung-Ung KangNeuroregeneration and Stem Cell Programs, Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD, United States.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The aggregation of α-synuclein in the nervous system leads to a class of neurodegenerative disorders termed α-synucleinopathies. A form of primary degenerative dementia called Lewy body dementia (LBD) often develops when these aggregations develop into intracellular inclusions called Lewy bodies (LB) and Lewy neurites (LN). Although high frequency of LBD are the leading cause of dementia after Alzheimer's disease (AD), limited information has been discovered about its pathological pathway or diagnostic criteria. In this report, we attempt to address such shortcomings via utilizing a proteomic approach to identify the proteome changes following intrastriatal injection of α-synuclein pre-formed fibril (α-syn PFF). Using mass spectrometry, we have identified a total of 179 proteins that were either up- or down-regulated at different time points, with the four proteins-TPP3, RAB10, CAMK2A, and DYNLL1, displaying the most significant changes throughout the timeframe. Through further examining the modulated proteins with network-based enrichment analyses, we have found that (1) the most significantly associated neurodegenerative pathways were Parkinson's (

Indexed as

Lewy body dementia (LBD)Parkinson's Disease with Dementiaquantitative proteomicssynucleinopathy modelsTMT-isobaric mass technique

Identifiers

PMID39529733
PMCPMC11552175

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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.