Evidence map›Paper›PMID 39108314›Full record

ArticleFrontiers in neuroscience2024

Polygenic scores and Mendelian randomization identify plasma proteins causally implicated in Alzheimer's disease.

Davis B Cammann, Yimei Lu, Jerome I Rotter, Alexis C Wood, Jingchun Chen

Abstract read
In one paragraph

Article in Frontiers in neuroscience, 2024. 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
  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

5 authors.

Davis B Cammann *Nevada Institute of Personalized Medicine, University of Nevada Las Vegas, Las Vegas, NV, United States.
Yimei Lu *Nevada Institute of Personalized Medicine, University of Nevada Las Vegas, Las Vegas, NV, United States.
Jerome I RotterThe Lundquist Institute for Biomedical Innovation, Harbor-UCLA Medical Center, Torrance, CA, United States.
Alexis C WoodBaylor College of Medicine, Houston, TX, United States.
Jingchun ChenNevada Institute of Personalized Medicine, University of Nevada Las Vegas, Las Vegas, NV, United States.

Funding

UCLA Clinical Translational Science InstituteUL1TR001881 · NCATS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ARLEEN F. BROWN, ARASH NAEIM · 2016 to 2026
$118.1M
Transgenic & Knock-out MouseP30DK063491 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI ALAN R. SALTIEL · 2003 to 2026
$40.4M
Tracking and EvaluationU54GM104944 · NIGMS · UNIVERSITY OF NEVADA LAS VEGAS · PI MARCHAND, GWEN · 2013 to 2023
$39.6M
Subclinical Vascular Contributions to Alzheimer's Disease: The Multi-Ethnic Study of Atherosclerosis (MESA) Multisite Study of AD (Renewal)R01AG058969 · NIA · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI Timothy M. Hughes, YONGMEI LIU · 2018 to 2026
$33.4M
The Genome Analysis and Sequencing Pipeline (GASP)P20GM121325 · NIGMS · UNIVERSITY OF NEVADA LAS VEGAS · PI CHEN, JINGCHUN · 2018 to 2022
$11.5M
CHARGE Consortium: Omics Discovery for CVD and Aging PhenotypesR01HL105756 · NHLBI · UNIVERSITY OF WASHINGTON · PI Bruce M Psaty, NICHOLAS L SMITH · 2011 to 2026
$9.5M
Convolutional Neural Network for Disease Prediction, Biomarker Discovery, and Validation in Alzheimer's DiseaseR15AG083618 · NIA · UNIVERSITY OF NEVADA LAS VEGAS · PI Jingchun Chen · 2024 to 2026
$751k
NCATS NIH HHS UL1 TR001881NHLBI NIH HHS R01 HL105756NIA NIH HHS R01 AG058969NIA NIH HHS R15 AG083618NIDDK NIH HHS P30 DK063491NIGMS NIH HHS P20 GM121325NIGMS NIH HHS U54 GM104944
6 · The paper itself

Abstract

Background: An increasing body of evidence suggests that neuroinflammation is one of the key drivers of late-onset Alzheimer's disease (LOAD) pathology. Due to the increased permeability of the blood-brain barrier (BBB) in older adults, peripheral plasma proteins can infiltrate the central nervous system (CNS) and drive neuroinflammation through interactions with neurons and glial cells. Because these inflammatory factors are heritable, a greater understanding of their genetic relationship with LOAD could identify new biomarkers that contribute to LOAD pathology or offer protection against it. Methods: We used a genome-wide association study (GWAS) of 90 different plasma proteins ( Results: We identified four plasma protein level PGSs that were significantly associated (FDR-adjusted Conclusion: Our results show that plasma HGF has a negative causal relationship with LOAD liability that is driven by pleiotropic SNPs possibly involved in other pathways. These findings suggest a low transferability between PGS and MR approaches, and future research should explore ways in which LOAD and the plasma proteome may interact.

Indexed as

Alzheimer’s diseaseMendelian randomizationplasma proteinspolygenic scorepQTL

Identifiers

PMID39108314
PMCPMC11300309

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.