Evidence map›Paper›PMID 40076979›Full record

ArticleInternational journal of molecular sciences2025

Differential Transcriptional Programs Reveal Modular Network Rearrangements Associated with Late-Onset Alzheimer's Disease.

Alejandra Paulina Pérez-González, Guillermo de Anda-Jáuregui, Enrique Hernández-Lemus

Abstract read
In one paragraph

Article in International journal of molecular sciences, 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. Canonical Pathways Rewiring in Alzheimer's Disease.International journal of molecular sciences · 2026
    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

3 authors.

Alejandra Paulina Pérez-GonzálezDivisión de Genómica Computacional, Instituto Nacional de Medicina Genómica, Mexico City 14610, Mexico.ORCID 0000-0001-7352-4444
Guillermo de Anda-JáureguiDivisión de Genómica Computacional, Instituto Nacional de Medicina Genómica, Mexico City 14610, Mexico.ORCID 0000-0002-7749-0365
Enrique Hernández-LemusDivisión de Genómica Computacional, Instituto Nacional de Medicina Genómica, Mexico City 14610, Mexico.ORCID 0000-0002-1872-1397

Funding

Alzheimer's Disease Genetics ConsortiumU01AG032984 · NIA · UNIVERSITY OF PENNSYLVANIA · PI SCHELLENBERG, GERARD DAVID · 2009 to 2024
$60.4M
SUPPLEMENT TO RUSH ALZHEIMERS DISEASE CENTER COREP30AG010161 · NIA · RUSH UNIVERSITY MEDICAL CENTER · PI BENNETT, DAVID ALAN · 1991 to 2020
$49.1M
EPIDEMIOLOGY OF NEURAL RESERVE AND NEUROBIOLOGY IN AGINGR01AG017917 · NIA · RUSH UNIVERSITY MEDICAL CENTER · PI BENNETT, DAVID ALAN · 2001 to 2023
$43.3M
RISK FACTORS, PATHOLOGY, AND CLINICAL EXPRESSIONS OF ADR01AG015819 · NIA · RUSH UNIVERSITY MEDICAL CENTER · PI BENNETT, DAVID ALAN · 1998 to 2024
$21.4M
Multi-omic network-directed proteoform discovery, dissection and functional validation to prioritize novel AD therapeutic targetsU01AG061356 · NIA · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI BENNETT, DAVID ALAN, DE JAGER, PHILIP L · 2018 to 2022
$13.7M
Pathway discovery, validation and compound identification for Alzheimer's disease - SupplementU01AG046152 · NIA · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI BENNETT, DAVID ALAN, DE JAGER, PHILIP L · 2013 to 2017
$13.6M
Discovery of Novel Proteomic Targets in Alzheimer's DiseaseU01AG046161 · NIA · EMORY UNIVERSITY · PI BENNETT, DAVID ALAN, GESCHWIND, DANIEL H · 2014 to 2018
$8.4M
Genetic Epidemiology of Cognitive Decline in an Aging Population SampleR01AG030146 · NIA · RUSH UNIVERSITY MEDICAL CENTER · PI EVANS, DENIS A · 2007 to 2018
$6.2M
Exploring the Role of the Brain Epigenome: Cognitive Decline and Life ExperiencesR01AG036042 · NIA · RUSH UNIVERSITY MEDICAL CENTER · PI BENNETT, DAVID ALAN · 2009 to 2013
$4.1M
Deconstructing and modeling the single cell architecture of the Alzheimer brainRF1AG057473 · NIA · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI BENNETT, DAVID ALAN, DE JAGER, PHILIP L · 2017 to 2018
$4.0M
Exploring the Role of the Brain Transcriptome in Cognitive DeclineR01AG036836 · NIA · BRIGHAM AND WOMEN'S HOSPITAL · PI DE JAGER, PHILIP L · 2011 to 2014
$2.9M
Identifying, validating and targeting AD susceptibility networks in monocytesR01AG048015 · NIA · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI DE JAGER, PHILIP L · 2014 to 2018
$1.9M
Consejo Nacional de Humanidades, Ciencias y Tecnologías 904078NIA NIH HHS P30 AG010161NIA NIH HHS R01 AG015819NIA NIH HHS R01 AG017917NIA NIH HHS R01 AG030146NIA NIH HHS R01 AG036042NIA NIH HHS R01 AG036836NIA NIH HHS R01 AG048015NIA NIH HHS RC2 AG036547NIA NIH HHS RF1 AG057473NIA NIH HHS U01 AG032984NIA NIH HHS U01 AG046152NIA NIH HHS U01 AG046161NIA NIH HHS U01 AG061356
6 · The paper itself

Abstract

Alzheimer's disease (AD) is a complex, genetically heterogeneous disorder. The diverse phenotypes associated with AD result from interactions between genetic and environmental factors, influencing multiple biological pathways throughout disease progression. Network-based approaches offer a way to assess phenotype-specific states. In this study, we calculated key network metrics to characterize the network transcriptional structure and organization in LOAD, focusing on genes and pathways implicated in AD pathology within the dorsolateral prefrontal cortex (DLPFC). Our findings revealed disease-specific coexpression markers associated with diverse metabolic functions. Additionally, significant differences were observed at both the mesoscopic and local levels between AD and control networks, along with a restructuring of gene coexpression and biological functions into distinct transcriptional modules. These results show the molecular reorganization of the transcriptional program occurring in LOAD, highlighting specific adaptations that may contribute to or result from cellular responses to pathological stressors. Our findings may support the development of a unified model for the causal mechanisms of AD, suggesting that its diverse manifestations arise from multiple pathways working together to produce the disease's complex clinical patho-phenotype.

Indexed as

Alzheimer DiseaseGene Regulatory NetworksTranscription, GeneticAgedFemaleGene Expression ProfilingGene Expression RegulationHumansMalePrefrontal CortexTranscriptomeAlzheimer’s diseasegene co-expression networksLOADnetwork analytics

Identifiers

PMID40076979
PMCPMC11900169

What OpenQuestion holds

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Registered trials

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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.