Evidence mapPaperPMID 41588241Full record

ArticleMolecular neurobiology2026

Exploratory RNA Sequencing Reveals Systemic Metabolic Dysregulation in Alzheimer's Disease: Insights from a Diverse Latin American Cohort.

Lina M Villegas-Trujillo, Beatriz Parra, Diana López-Álvarez, Lina M Gonzalez-Ojeda, Alejandra Torres-Parga, Sebastián Cardona, Nelson Rivera-Franco, Juan F Cardona

Abstract read
In one paragraph

Article in Molecular neurobiology, 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.

Lina M Villegas-TrujilloPhD Program in Biomedical Sciences, School of Basic Sciences, Faculty of Health, Universidad del Valle, Cali, Colombia.ORCID http://orcid.org/0000-0002-4568-6697
Beatriz ParraSchool of Basic Sciences, Department of Microbiology, Faculty of Health, Universidad del Valle, Cali, Colombia.
Diana López-ÁlvarezDepartment of Biological Sciences, Faculty of Agricultural Sciences, Universidad Nacional de Colombia, Palmira, Colombia.
Lina M Gonzalez-OjedaPhD Program in Psychology, Faculty of Psychology, Universidad del Valle, Cali, Colombia.
Alejandra Torres-PargaPhD Program in Psychology, Faculty of Psychology, Universidad del Valle, Cali, Colombia.
Sebastián CardonaNeurology Residency Program, Department of Internal Medicine, Faculty of Health, Universidad del Valle, Cali, Colombia.
Nelson Rivera-FrancoSchool of Basic Sciences, Department of Microbiology, Faculty of Health, Universidad del Valle, Cali, Colombia.
Juan F CardonaDepartment of Developmental Science, Cognition and Neuroscience, Faculty of Psychology, Universidad del Valle, Calle 13 No. 100-00, Edificio 388 Oficina 4035, Cali, Colombia. felipe.cardona@correounivalle.edu.co.ORCID http://orcid.org/0000-0001-6795-7753

Funding

Sistema General de Regalías de Colombia BPIN2018000100059U.S. National Institutes of Health R01-NS110122
6 · The paper itself

Abstract

Alzheimer's disease (AD) is characterized by an insidious onset and complex pathophysiology, necessitating the development of effective strategies for early detection and intervention. This exploratory study aimed to identify differentially expressed genes (DEGs) and disrupted molecular pathways in AD by analyzing blood samples from participants recruited in Valle del Cauca, Colombia, a region with high genetic admixture and persistent underrepresentation in genomic research. A total of 41 individuals (AD, n = 14; cognitively healthy controls (CHC), n = 27) were included. Groups did not differ significantly in age, education, sex distribution, or vascular comorbidities. Peripheral blood RNA was sequenced using 150-bp paired-end reads, and transcriptomic profiling revealed 399 DEGs, with 378 upregulated and 21 downregulated in the AD group. Key genes such as APOE, MMP2, PPARG, and TUBB3 were enriched in the Metabolism of Proteins pathway. At the same time, TUBB3, CACNA2D1, and GABBR2 were implicated in transmission across chemical synapses, suggesting synaptic signaling and protein metabolism dysregulation. Multiple factor analysis (MFA), integrating gene expression with neurocognitive and functional outcomes, revealed distinct molecular signatures associated with cognitive decline and functional impairment. These findings highlight the role of systemic metabolic dysfunction and synaptic dysregulation in AD pathogenesis. By focusing on an ancestrally diverse cohort, this study underscores the critical need to expand the molecular characterization of AD beyond European-ancestry populations, informing the development of inclusive biomarkers and precision strategies for early diagnosis and intervention.

Indexed as

Alzheimer DiseaseSequence Analysis, RNAAgedCohort StudiesFemaleGene Expression ProfilingHumansLatin AmericaMaleTranscriptomeAlzheimer’s diseaseCognitive dysfunctionGene expression profilingRNA-Seq

Identifiers

PMID41588241
PMCPMC12835041

What Socratic 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 Socratic graph.