Evidence map›Paper›PMID 42883949›Full record

ArticleInternational journal of molecular sciences2026

Age-Stratified Analysis of Blood-Brain Barrier Proteins Identifies Lower Occludin Abundance in the 3xTg-AD Model.

Karen Michelle Delgado-Minjares, Catalina Flores-Maldonado, Jessica Paulina Campos-Blázquez, Sofía Y Díaz-Miranda, Jesús Andrade-Guerrero, Wendolin Colín-García, Karen León-Arcia, Daniel Martinez-Fong, Rubén G Contreras, Luis O Soto-Rojas

Abstract read
In one paragraph

Article in International journal of molecular sciences, 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

10 authors.

Karen Michelle Delgado-MinjaresDepartamento de Fisiología, Biofísica y Neurociencias, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional, Ciudad de México C.P. 07360, Mexico.ORCID 0000-0001-8321-0705
Catalina Flores-MaldonadoDepartamento de Fisiología, Biofísica y Neurociencias, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional, Ciudad de México C.P. 07360, Mexico.ORCID 0000-0002-5816-0694
Jessica Paulina Campos-BlázquezDepartamento de Fisiología, Biofísica y Neurociencias, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional, Ciudad de México C.P. 07360, Mexico.
Sofía Y Díaz-MirandaDepartamento de Neurobiología del Desarrollo y Neurofisiología, Instituto de Neurobiología, Universidad Nacional Autónoma de México, Querétaro C.P. 76230, Mexico.ORCID 0000-0002-3354-2717
Jesús Andrade-GuerreroLaboratorio de Investigación en Neurociencias, Envejecimiento y Neurodegeneración (LINEN), Carrera de Médico Cirujano, Facultad de Estudios Superiores Iztacala, Universidad Nacional Autónoma de México, Ciudad de México C.P. 54090, Mexico.ORCID 0000-0002-0574-8814
Wendolin Colín-GarcíaLaboratorio de Investigación en Neurociencias, Envejecimiento y Neurodegeneración (LINEN), Carrera de Médico Cirujano, Facultad de Estudios Superiores Iztacala, Universidad Nacional Autónoma de México, Ciudad de México C.P. 54090, Mexico.
Karen León-ArciaLaboratorio de Investigación en Neurociencias, Envejecimiento y Neurodegeneración (LINEN), Carrera de Médico Cirujano, Facultad de Estudios Superiores Iztacala, Universidad Nacional Autónoma de México, Ciudad de México C.P. 54090, Mexico.ORCID 0000-0001-5143-1642
Daniel Martinez-FongDepartamento de Fisiología, Biofísica y Neurociencias, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional, Ciudad de México C.P. 07360, Mexico.ORCID 0000-0002-2934-8380
Rubén G ContrerasDepartamento de Fisiología, Biofísica y Neurociencias, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional, Ciudad de México C.P. 07360, Mexico.ORCID 0000-0001-7311-1615
Luis O Soto-RojasLaboratorio de Investigación en Neurociencias, Envejecimiento y Neurodegeneración (LINEN), Carrera de Médico Cirujano, Facultad de Estudios Superiores Iztacala, Universidad Nacional Autónoma de México, Ciudad de México C.P. 54090, Mexico.ORCID 0000-0002-5013-3608

Funding

Ciencia básica y de Frontera 2019/7357Ciencia básica y de Frontera CBF-2025-G35the Universidad Nacional Autónoma de México through the Programa de Apoyo a Proyectos de Investigación e Innovación Tecnológica IN227026Universidad Nacional Autónoma de México through the Programa de Apoyo a Proyectos de Investigación e Innovación Tecnológica 20932
6 · The paper itself

Abstract

Alzheimer's disease (AD) is a progressive neurodegenerative disorder in which blood-brain barrier (BBB) dysfunction may arise early. We performed an age-stratified, cross-sectional analysis of pericyte- and endothelial-associated markers and junctional proteins (claudin-1, -3, -5, occludin, and VE-cadherin) in cerebral capillary-enriched fractions from male Non-Tg and 3xTg-AD mice at asymptomatic, early, and advanced stages (3, 6, 12, and 16 months of age). Protein abundance was assessed by Western blot, and BBB permeability to 3-5 kDa FITC-dextran was evaluated at 3 months in an independent cohort. At 3 months, the pSRC/SRC ratio and an MMP-9-immunoreactive band were also evaluated in a separate cohort as candidate signaling markers related to occludin dysregulation. We detected no significant age or genotype effects for the pericyte- and endothelial-associated markers or for most junctional protein outcomes. Occludin was the only protein outcome with a significant overall genotype effect, with the largest mean reductions observed at 3 (~80%) and 6 months (~68%). A small exploratory cohort showed a higher hemisphere-derived permeability index in 3xTg-AD mice at 3 months. Neither pSRC/SRC nor the abundance of the MMP-9-immunoreactive band differed significantly between genotypes. These findings identify lower occludin abundance as the principal BBB-associated protein alteration in the 3xTg-AD model and provide exploratory evidence of increased BBB permeability at 3 months. These independent observations warrant longitudinal and translational evaluation to determine whether occludin abundance and BBB permeability could serve as indicators of early neurovascular dysfunction in AD.

Indexed as

Alzheimer DiseaseBlood-Brain BarrierOccludinAgingAnimalsCadherinsDisease Models, AnimalEndothelial CellsHumansMaleMiceMice, TransgenicPericytesCadherinsOccludinOcln protein, mouseAlzheimer’s diseasecapillary brain proteinsendothelial cellsmouse modeltight junctions

Identifiers

PMID42883949
PMCPMC13665031

What OpenQuestion holds

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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.