Evidence map›Paper›PMID 39623717›Full record

ArticleCurrent Alzheimer research2026

Quantitative Proteomic Analysis of APP/PS1 Transgenic Mice.

Jiayuan Wang, Xinyu Wang, Zihui An, Xuan Wang, Yaru Wang, Yuehan Lu, Mengsheng Qiu, Zheqi Liu, Zhou Tan

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In one paragraph

Article in Current Alzheimer research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed, 1 pooled it
–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 synthesis or guideline pooled it.

  1. Pooled it
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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

9 authors.

Jiayuan WangZhejiang Key Laboratory of Organ Development and Regeneration, School of Life and Environmental Science, Hangzhou Normal University, Hangzhou , 311121, China.
Xinyu WangZhejiang Key Laboratory of Organ Development and Regeneration, School of Life and Environmental Science, Hangzhou Normal University, Hangzhou , 311121, China.
Zihui AnZhejiang Key Laboratory of Organ Development and Regeneration, School of Life and Environmental Science, Hangzhou Normal University, Hangzhou , 311121, China.
Xuan WangZhejiang Key Laboratory of Organ Development and Regeneration, School of Life and Environmental Science, Hangzhou Normal University, Hangzhou , 311121, China.
Yaru WangZhejiang Key Laboratory of Organ Development and Regeneration, School of Life and Environmental Science, Hangzhou Normal University, Hangzhou , 311121, China.
Yuehan LuZhejiang Key Laboratory of Organ Development and Regeneration, School of Life and Environmental Science, Hangzhou Normal University, Hangzhou , 311121, China.
Mengsheng QiuZhejiang Key Laboratory of Organ Development and Regeneration, School of Life and Environmental Science, Hangzhou Normal University, Hangzhou , 311121, China.
Zheqi LiuZhejiang Chinese Medical University, Hangzhou TCM Hospital, Hangzhou, 311121, China.
Zhou TanZhejiang Key Laboratory of Organ Development and Regeneration, School of Life and Environmental Science, Hangzhou Normal University, Hangzhou , 311121, China.ORCID 0000-0002-5071-7945

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAlzheimer's disease (AD) is a prevalent neurodegenerative disorder affecting the central nervous system (CNS), with its etiology still shrouded in uncertainty. The interplay of extracellular amyloid-β (Aβ) deposition, intracellular neurofibrillary tangles (NFTs) composed of tau protein, cholinergic neuronal impairment, and other pathogenic factors is implicated in the progression of AD.

objectiveThe current study endeavors to delineate the proteomic landscape alterations in the hippocampus of an AD murine model, utilizing proteomic analysis to identify key physiological and pathological shifts induced by the disease. This endeavor aims to shed light on the underlying pathogenic mechanisms, which could facilitate early diagnosis and pave the way for novel therapeutic interventions for AD.

methodsTo dissect the proteomic perturbations induced by Aβ and Presenilin-1 (PS1) in the AD pathogenesis, we undertook a label-free quantitative (LFQ) proteomic analysis focusing on the hippocampal proteome of the APP/PS1 transgenic mouse model. Employing a multi-faceted approach that included differential protein functional enrichment, cluster analysis, and protein-protein interaction (PPI) network analysis, we conducted a comprehensive comparative proteomic study between APP/PS1 transgenic mice and their wild-type C57BL/6 counterparts.

resultsMass spectrometry identified a total of 4817 proteins in the samples, with 2762 proteins being quantifiable. Comparative analysis revealed 396 proteins with differential expression between the APP/PS1 and control groups. Notably, 35 proteins exhibited consistent temporal regulation trends in the hippocampus, with concomitant alterations in biological pathways and PPI networks.

conclusionsThis study presents a comparative proteomic profile of transgenic (APP/PS1) and wild-type mice, highlighting the proteomic divergences. Furthermore, it charts the trajectory of proteomic changes in the AD mouse model across the developmental stages from 2 to 12 months, providing insights into the physiological and pathological implications of the disease-associated genetic mutations.

Indexed as

Alzheimer DiseaseAmyloid beta-Protein PrecursorHippocampusPresenilin-1ProteomeProteomicsAnimalsDisease Models, AnimalMiceMice, Inbred C57BLMice, TransgenicAmyloid beta-Protein PrecursorPresenilin-1ProteomeAlzheimer's diseaseAPP/PS1ferroptosishippocampusmitophagyproteomics

Identifiers

PMID39623717

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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.