Evidence mapPaperPMID 42097270Full record

ArticleMolecular & cellular proteomics : MCP2026

An Integrative Proteomic Approach to Reveal Altered Signaling Modules During Alzheimer's Disease Progression in PS19 Tauopathy Mice.

Eunji Cho, Seulah Lee, Hagyeong Lee, Jaehoon Kim, Yang Woo Kwon, Hyang-Sook Hoe, Dayea Kim, Jong Hyuk Yoon

Abstract read
In one paragraph

Article in Molecular & cellular proteomics : MCP, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Eunji ChoNeurodegenerative Diseases Research Group, Korea Brain Research Institute, Daegu, Republic of Korea; AI-based Neurodevelopmental Diseases Digital Therapeutics Group, Korea Brain Research Institute, Daegu, Republic of Korea.
Seulah LeeNeurodegenerative Diseases Research Group, Korea Brain Research Institute, Daegu, Republic of Korea.
Hagyeong LeeNeurodegenerative Diseases Research Group, Korea Brain Research Institute, Daegu, Republic of Korea.
Jaehoon KimNeurodegenerative Diseases Research Group, Korea Brain Research Institute, Daegu, Republic of Korea.
Yang Woo KwonNew Drug Development Center, Daegu-Gyeongbuk Medical Innovation Foundation (K-MEDI hub), Daegu, Republic of Korea.
Hyang-Sook HoeAI-based Neurodevelopmental Diseases Digital Therapeutics Group, Korea Brain Research Institute, Daegu, Republic of Korea.
Dayea KimNew Drug Development Center, Daegu-Gyeongbuk Medical Innovation Foundation (K-MEDI hub), Daegu, Republic of Korea.
Jong Hyuk YoonNeurodegenerative Diseases Research Group, Korea Brain Research Institute, Daegu, Republic of Korea. Electronic address: jhyoon@kbri.re.kr.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is a slowly progressive neurodegenerative disease that is characterized by cognitive, functional, and behavioral impairments. These changes occur owing to the progressive accumulation of extracellular amyloid-beta plaques and intracellular neurofibrillary tangles of hyperphosphorylated tau protein. AD is associated with the dysfunction of several essential neurotransmitter systems, such as dopamine, and impaired neurotransmission. Despite the association of neurotransmitter changes within the brain and AD pathology, in-depth profiling studies on neurotransmitters and their related proteomic changes are limited. This study was conducted to profile and integrate the proteomes and neurotransmitters in seven brain regions of PS19 (Tau P301S) mice according to AD progression between 4 and 7 months. Proteomic analysis revealed significantly altered canonical pathways in various brain regions, including metabolic abnormalities. In the neurotransmitter profile, we found significant alterations in the levels of six neurotransmitters-dopamine, serotonin, homovanillic acid, norepinephrine, 3-methoxytyramine, and 3,4-dihydroxyphenylacetic acid-during AD progression. Using an integrative approach between proteome and neurotransmitter profiles, we found that AD progression-dependent dopamine- and serotonin-related signaling modules are closely related to neurotransmitter changes, especially in the hippocampus and cerebellum. This integrative approach could provide new signaling modules to help understand AD progression and thereby enable improved treatment and clinical outcomes.

Indexed as

Alzheimer DiseaseProteomicsSignal TransductionTauopathiesAnimalsBrainDisease ProgressionDopamineHippocampusMiceMice, TransgenicNeurotransmitter AgentsProteometau ProteinsDopamineNeurotransmitter AgentsProteometau ProteinsAlzheimer’s diseasedementiaintegrative proteomic approachsignaling modules

Identifiers

PMID42097270
PMCPMC13241738

What Socratic 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 Socratic graph.