Evidence map›Paper›PMID 40662549›Full record

ArticleCurrent Alzheimer research2025

Identification of MicroRNA Drug Targets for Alzheimer's and Diabetes Mellitus Using Network Medicine.

Ricardo Castillo-Velazquez, Julio E Castaneda-Delgado, Mariana H Garcia-Hernandez, Bruno Rivas-Santiago, Sofia Ruiz-Hernandez, Eyra Liliana Ortiz-Perez, Juan C Lopez-Alvarenga, Gildardo Rivera, Edgar E Lara-Ramirez

Abstract read
PubMed Publisher
In one paragraph

Article in Current Alzheimer research, 2025. 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

9 authors.

Ricardo Castillo-VelazquezCentro de Investigación en Ciencias de la Salud y Biomedicina, Universidad Autónoma de San Luis Potosí, San Luis Potosí, México.
Julio E Castaneda-DelgadoUnidad de Investigación Biomédica de Zacatecas, Instituto Mexicano del Seguro Social, Zacatecas, México.
Mariana H Garcia-HernandezUnidad de Investigación Biomédica de Zacatecas, Instituto Mexicano del Seguro Social, Zacatecas, México.
Bruno Rivas-SantiagoUnidad de Investigación Biomédica de Zacatecas, Instituto Mexicano del Seguro Social, Zacatecas, México.
Sofia Ruiz-HernandezCentro de Investigación en Ciencias de la Salud y Biomedicina, Universidad Autónoma de San Luis Potosí, San Luis Potosí, México.
Eyra Liliana Ortiz-PerezLaboratorio de Biotecnología Farmacéutica, Centro de Biotecnología Genómica, Instituto Politécnico Nacional, Reynosa, Tamaulipas, México.
Juan C Lopez-AlvarengaDivision of Population Health and Biostatistics, School of Medicine, The University of Texas Rio Grande Valley, Texas, Edinburg, United States of America.
Gildardo RiveraLaboratorio de Biotecnología Farmacéutica, Centro de Biotecnología Genómica, Instituto Politécnico Nacional, Reynosa, Tamaulipas, México.
Edgar E Lara-RamirezLaboratorio de Biotecnología Farmacéutica, Centro de Biotecnología Genómica, Instituto Politécnico Nacional, Reynosa, Tamaulipas, México.

Funding

CONACyT 320004
6 · The paper itself

Abstract

introductionType 2 diabetes mellitus (T2D) is a known risk factor for developing Alzheimer's disease (AD). Recent research shows that both diseases share complex and related pathophysiological processes. Network medicine approaches can help to elucidate common dysregulated processes among different diseases, such as AD and T2D. Thus, the aim of this work was to determine differentially expressed genes (DEGs) in AD and T2D and to apply a network medicine approach to identify the microRNAs (miRNAs) involved in the AD-T2D association.

methodsGene expression microarray data sets consisting of 384 control samples and 399 samples belonging to AD and T2D disease were analyzed to obtain DEGs shared by both diseases; the miRNAs associated with these DEGs were predicted using a network medicine approach. Finally, potential small molecules targeting these potentially deregulated miRNAs were identified.

resultsAD and T2D shared a subset of 82 downregulated DEGs. These genes were significantly associated (p < 0.01) with the ontology terms of chemical synaptic deregulation. DEGs were associated with 12 miRNAs expressed in specific tissues for AD and T2D. Such miRNAs were also primarily associated with the ontology terms related to synaptic deregulation and cancer, and AKT signaling pathways. Steroid anti-inflammatory drugs, antineoplastics, and glucose metabolites were predicted to be potential regulators of the 12 shared miRNAs. DISCUSSION: The network medicine approach integrating DEGs and miRNAs enabled the identification of shared, potentially deregulated biological processes and pathways underlying the pathophysiology of AD and T2D. These common molecular mechanisms were also linked to drugs currently used in clinical practice, suggesting that this strategy may inform future drug repurposing efforts. Nonetheless, further in-depth biological validation is required to confirm these findings.

conclusionNetwork medicine allowed identifying 12 miRNAs involved in the AD-T2D association, and these could be drug targets for the design of new treatments; however, the identified miRNAs need further experimental confirmation.

Indexed as

Alzheimer DiseaseDiabetes Mellitus, Type 2Gene Regulatory NetworksMicroRNAsGene Expression ProfilingHumansMicroRNAsAlzheimer's diseasediabetes mellitusdrug designmetabolic disorder.microRNAsNetwork medicine

Identifiers

What Socratic holds

Textmetadata
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.