Evidence map›Paper›PMID 40345165›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025

In-Depth Cell-Type-Specific Proteome Landscape of the Brain from Human Amyloid-β Overexpression Mouse Model.

Taekyung Ryu, Seok-Young Kim, Thujitha Thuraisamy, Jisu Shin, Yura Jang, Tae-In Kam, Chan Hyun Na

Abstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. 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. Article
  2. 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

7 authors.

Taekyung RyuDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA.
Seok-Young KimDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA.
Thujitha ThuraisamyDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA.
Jisu ShinDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA.
Yura JangDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA.
Tae-In KamDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA.
Chan Hyun NaDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA.ORCID https://orcid.org/0000-0002-3622-2938

Funding

Region-Specific Vulnerability of the Lewy Body Dementia's BrainR01NS123456 · NINDS · JOHNS HOPKINS UNIVERSITY · PI KAM, TAE-IN, KANG, SUNG UNG · 2021 to 2025
$3.6M
Fourier Transform Orbitrap Fusion Lumos Tribrid Mass Spectrometer with ETDS10OD021844 · OD · JOHNS HOPKINS UNIVERSITY · PI PANDEY, AKHILESH · 2016 to 2016
$1.1M
Helis Foundation 139891Helis Foundation 143504Ministry of Health & Welfare and Ministry of Science and ICT, Republic of Korea RS-2024-00358266NIH HHS R01NS123456NIH HHS S10 OD021844NIH HHS S10OD021844NINDS NIH HHS R01 NS123456
6 · The paper itself

Abstract

Amyloid-β (Aβ) plays a crucial role in Alzheimer's disease pathogenesis. Understanding how Aβ overexpression alters the proteome of individual brain cell types is essential but challenging due to the nature of brain tissue, which contains intermingled various cell types. The current methods for cell-type-specific proteomics either require genetic modifications or complex cell isolation, limiting their use. This study introduces a novel method, in situ cell-type-specific proteome analysis using antibody-mediated biotinylation (iCAB), which applies immunohistochemistry with biotin-tyramide to target cell-specific proteins directly in tissue. Applied to 5xFAD mice, iCAB enables us to identify ≈8000 cell-type-specific proteomes with significantly more differentially expressed proteins than traditional bulk proteome methods, pinpointing unique pathways such as mRNA processing, calcium regulation, and phagocytosis for neurons, astrocytes, and microglia, respectively. This study reports in-depth the cell-type-specific brain proteome landscape of the human Aβ overexpression mouse model for the first time using an innovative tool that is powerful, straightforward, and applicable to both animal models and human tissues, without the need for prior genetic alterations.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesBrainProteomeAnimalsAstrocytesDisease Models, AnimalHumansMiceMice, TransgenicMicrogliaNeuronsProteomicsAmyloid beta-PeptidesProteomebiotin‐tyramidesbiotinylationbrainscell‐type‐specific proteomesiCABimmunohistochemistrymass spectrometry

Identifiers

PMID40345165
PMCPMC12120748

What OpenQuestion holds

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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.