Evidence map›Paper›PMID 35944844›Full record

ArticleMolecular & cellular proteomics : MCP2022

Temporal and Sex-Linked Protein Expression Dynamics in a Familial Model of Alzheimer's Disease.

Filipa Blasco Tavares Pereira Lopes, Daniela Schlatzer, Rihua Wang, Xiaolin Li, Emily Feng, Mehmet Koyutürk, Xin Qi, Mark R Chance

Abstract read
In one paragraph

Article in Molecular & cellular proteomics : MCP, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing 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

12 citing papers in PubMed.

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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

8 authors.

Filipa Blasco Tavares Pereira LopesDepartment of Nutrition, School of Medicine, Case Western Reserve University, Cleveland, Ohio, USA; Center for Proteomics and Bioinformatics, School of Medicine, Case Western Reserve University, Cleveland, Ohio, USA.
Daniela SchlatzerDepartment of Nutrition, School of Medicine, Case Western Reserve University, Cleveland, Ohio, USA; Center for Proteomics and Bioinformatics, School of Medicine, Case Western Reserve University, Cleveland, Ohio, USA.
Rihua WangDepartment of Physiology & Biophysics, School of Medicine, Case Western Reserve University, Cleveland, Ohio, USA; Center for Mitochondrial Diseases, School of Medicine, Case Western Reserve University, Cleveland, Ohio, USA.
Xiaolin LiDepartment of Nutrition, School of Medicine, Case Western Reserve University, Cleveland, Ohio, USA; Center for Proteomics and Bioinformatics, School of Medicine, Case Western Reserve University, Cleveland, Ohio, USA.
Emily FengDepartment of Nutrition, School of Medicine, Case Western Reserve University, Cleveland, Ohio, USA; Center for Proteomics and Bioinformatics, School of Medicine, Case Western Reserve University, Cleveland, Ohio, USA.
Mehmet KoyutürkCenter for Proteomics and Bioinformatics, School of Medicine, Case Western Reserve University, Cleveland, Ohio, USA; Department of Computer and Data Sciences, Case School of Engineering, Case Western Reserve University, Cleveland, Ohio, USA.
Xin QiDepartment of Physiology & Biophysics, School of Medicine, Case Western Reserve University, Cleveland, Ohio, USA; Center for Mitochondrial Diseases, School of Medicine, Case Western Reserve University, Cleveland, Ohio, USA.
Mark R ChanceDepartment of Nutrition, School of Medicine, Case Western Reserve University, Cleveland, Ohio, USA; Center for Proteomics and Bioinformatics, School of Medicine, Case Western Reserve University, Cleveland, Ohio, USA. Electronic address: mark.chance@case.edu.

Funding

Role of brain lipid metabolism in Alzheimer's diseaseR01AG065240 · NIA · CASE WESTERN RESERVE UNIVERSITY · PI QI, XIN · 2020 to 2024
$3.0M
Proteostasis dysregulation and alpha-synucleinR01NS115903 · NINDS · CASE WESTERN RESERVE UNIVERSITY · PI QI, XIN · 2020 to 2023
$2.4M
Regulation of CHCHD6 in Alzheimer's diseaseRF1AG074346 · NIA · CASE WESTERN RESERVE UNIVERSITY · PI QI, XIN · 2022 to 2022
$2.1M
Construction, Analysis, and Utilization of Co-Phosphorylation Networks to Characterize Cellular SignalingR01LM012980 · NLM · CASE WESTERN RESERVE UNIVERSITY · PI Marzieh Ayati, MARK R CHANCE · 2019 to 2026
$2.1M
Phospho Proteomics Alzheimers SupplementR01GM117208 · NIGMS · CASE WESTERN RESERVE UNIVERSITY · PI CHANCE, MARK R · 2016 to 2018
$1.4M
Orbitrap Fusion Lumos Tribrid Mass SpectrometerS10OD026882 · OD · CASE WESTERN RESERVE UNIVERSITY · PI CHANCE, MARK R · 2019 to 2019
$1.0M
Q Exactive HF-X hybrid quadrupole-Orbitrap mass spectrometer (QE HF-X)S10OD028614 · OD · CASE WESTERN RESERVE UNIVERSITY · PI CHANCE, MARK R · 2020 to 2020
$600k
NIA NIH HHS R01 AG065240NIA NIH HHS RF1 AG074346NIGMS NIH HHS R01 GM117208NIH HHS S10 OD026882NIH HHS S10 OD028614NINDS NIH HHS R01 NS115903NLM NIH HHS R01 LM012980
6 · The paper itself

Abstract

Mouse models of Alzheimer's disease (AD) show progression through stages reflective of human pathology. Proteomics identification of temporal and sex-linked factors driving AD-related pathways can be used to dissect initiating and propagating events of AD stages to develop biomarkers or design interventions. In the present study, we conducted label-free proteome measurements of mouse hippocampus tissue with variables of time (3, 6, and 9 months), genetic background (5XFAD versus WT), and sex (equal males and females). These time points are associated with well-defined phenotypes with respect to the following: Aβ42 plaque deposition, memory deficits, and neuronal loss, allowing correlation of proteome-based molecular signatures with the mouse model stages. Our data show 5XFAD mice exhibit increases in known human AD biomarkers as amyloid-beta peptide, APOE, GFAP, and ITM2B are upregulated across all time points/stages. At the same time, 23 proteins are here newly associated with Alzheimer's pathology as they are also dysregulated in 5XFAD mice. At a pathways level, the 5XFAD-specific upregulated proteins are significantly enriched for DNA damage and stress-induced senescence at 3-month only, while at 6-month, the AD-specific proteome signature is altered and significantly enriched for membrane trafficking and vesicle-mediated transport protein annotations. By 9-month, AD-specific dysregulation is also characterized by significant neuroinflammation with innate immune system, platelet activation, and hyper-reactive astrocyte-related enrichments. Aside from these temporal changes, analysis of sex-linked differences in proteome signatures uncovered novel sex and AD-associated proteins. Pathway analysis revealed sex-linked differences in the 5XFAD model to be involved in the regulation of well-known human AD-related processes of amyloid fibril formation, wound healing, lysosome biogenesis, and DNA damage. Verification of the discovery results by Western blot and parallel reaction monitoring confirm the fundamental conclusions of the study and poise the 5XFAD model for further use as a molecular tool for understanding AD.

Indexed as

Alzheimer DiseaseAmyloidAmyloid beta-PeptidesAnimalsApolipoproteins EBiomarkersDisease Models, AnimalFemaleHumansMaleMiceMice, TransgenicProteomeAmyloidAmyloid beta-PeptidesApolipoproteins EBiomarkersProteome5XFADAlzheimer's DiseasePathway analysisProteomeSex differencesTemporal dynamics

Identifiers

PMID35944844
PMCPMC9483563

What OpenQuestion holds

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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.