Evidence map›Paper›PMID 42498838›Full record

SynthesisNeurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology2026

Proteome-wide Mendelian randomization identifies causal plasma proteins in frontotemporal dementia.

Yuan Yao, Qin Zou, Ke Chen

Abstract readMeta-Analysis
PubMed Publisher
In one paragraph

Synthesis in Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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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

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3 · Its place in the literature

Who cites it

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4 · The record

Corrections and comments

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5 · Who and what money

Authors and funding

3 authors.

Yuan YaoDepartment of Cardiology, West China School of Public Health and West China Fourth Hospital, Sichuan University, 18th, Section 3, Renmin Road South, Wuhou District, Chengdu, Sichuan, 610041, China.
Qin ZouDepartment of Neurology, West China School of Public Health and West China Fourth Hospital, Sichuan University, Chengdu, Sichuan, 610041, China.
Ke ChenDepartment of Neurology, West China School of Public Health and West China Fourth Hospital, Sichuan University, Chengdu, Sichuan, 610041, China. chenke_scu@126.com.ORCID http://orcid.org/0009-0008-1067-083X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundFrontotemporal dementia (FTD) is a genetically and clinically heterogeneous neurodegenerative disorder with no disease-modifying treatments. Plasma proteomic signatures offer a promising avenue for uncovering disease mechanisms and developing targeted interventions.

methodsWe conducted protein-wide Mendelian randomization meta-analysis to explore causal relationships between plasma proteins and FTD and four subtypes, utilizing comprehensive datasets of protein quantitative trait loci.

resultsWe identified four plasma proteins significantly associated with FTD, namely RGS7 and ASAP2 (increased risk), as well as TMCC3 and VPS29 (decreased risk). Subtype-specific analyses revealed distinct protein signatures, including S100A13 and TREM1 in behavioral variant FTD, ING4 and TEX29 in FTD overlapping with motor neuron disease, SPINT2 in progressive non-fluent aphasia, and UGDH in semantic dementia.

conclusionsThis study implicates specific plasma proteins in FTD pathogenesis, with subtype-dependent effects. The identified proteins represent potential biomarkers for stratification and therapeutic targets.

Indexed as

Blood ProteinsFrontotemporal DementiaProteomeBiomarkersHumansMendelian Randomization AnalysisProteomicsQuantitative Trait LociBiomarkersBlood ProteinsProteomeFTDMendelian randomizationPlasma proteomicsPQTLTherapeutic targets

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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.