Evidence map›Paper›PMID 42278547›Full record

ArticleInternational journal of molecular sciences2026

Hippocampal, Microglial, Morphological, and Amyloid Profiles Following Thiamine Pyrophosphate Treatment in 3xTg-AD Mice.

Nelly Jovana Pastén-Castrejón, Humberto Martínez-Orozco, Gloria Yareli Gutiérrez-Silerio, Hebert Luis Hernández-Montiel, Juan Pablo Maya-Arteaga, Israel Poblano-Paez, Pablo García-Solís, Sofía Yolanda Díaz-Miranda

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. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Review
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.

Nelly Jovana Pastén-CastrejónLaboratorio de Endocrinología y Nutrición, Facultad de Medicina, Centro de Investigación Biomédica Avanzada de la Universidad Autónoma de Querétaro, Santiago de Querétaro 76140, Mexico.ORCID 0009-0009-0515-722X
Humberto Martínez-OrozcoDepartamento de Neurobiología del Desarrollo y Neurofisiología, Instituto de Neurobiología-UNAM Campus Juriquilla, Boulevard Juriquilla 3001, Querétaro 76230, Mexico.ORCID 0000-0002-7529-8476
Gloria Yareli Gutiérrez-SilerioLaboratorio de Endocrinología y Nutrición, Facultad de Medicina, Centro de Investigación Biomédica Avanzada de la Universidad Autónoma de Querétaro, Santiago de Querétaro 76140, Mexico.
Hebert Luis Hernández-MontielLaboratorio de Neurobiología y Bioingeniería Celular, Facultad de Ciencias Naturales de la Universidad Autónoma de Querétaro, Querétaro 76230, Mexico.
Juan Pablo Maya-ArteagaDepartamento de Neurobiología del Desarrollo y Neurofisiología, Instituto de Neurobiología-UNAM Campus Juriquilla, Boulevard Juriquilla 3001, Querétaro 76230, Mexico.ORCID 0009-0003-3570-9255
Israel Poblano-PaezDepartamento de Neurobiología del Desarrollo y Neurofisiología, Instituto de Neurobiología-UNAM Campus Juriquilla, Boulevard Juriquilla 3001, Querétaro 76230, Mexico.
Pablo García-SolísLaboratorio de Endocrinología y Nutrición, Facultad de Medicina, Centro de Investigación Biomédica Avanzada de la Universidad Autónoma de Querétaro, Santiago de Querétaro 76140, Mexico.ORCID 0000-0002-7483-0555
Sofía Yolanda Díaz-MirandaDepartamento de Neurobiología del Desarrollo y Neurofisiología, Instituto de Neurobiología-UNAM Campus Juriquilla, Boulevard Juriquilla 3001, Querétaro 76230, Mexico.ORCID 0000-0002-3354-2717

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is characterized by the accumulation of amyloid-β (Aβ) and chronic neuroinflammation, with microglia playing a central role in its pathogenesis. Alterations in microglial metabolism have been proposed to contribute to AD-related inflammatory responses and reduced Aβ clearance, suggesting that thiamine-dependent pathways may be relevant in this context. Thiamine pyrophosphate (TPP), the active form of vitamin B1, is essential for glucose metabolism and mitochondrial function; however, its association with microglial changes in AD remains unclear. In this study, 9-month-old female triple-transgenic AD (3xTg-AD) mice and non-transgenic controls (NoTg) received TPP (2.0 mg/mL) or saline as a vehicle for six weeks via osmotic pumps. Nesting, a hippocampus-dependent behavioral test, as well analyses of Aβ burden, microglial morphology, and the expression of genes related to metabolic and immune pathways were evaluated. Differences in nesting behavior between experimental groups were observed, but TPP treatment was not associated with an evident change in 3xTg-AD mice. In the subiculum and CA1 regions of the hippocampus of female 3xTg-AD mice exposed to TPP, a lower Aβ burden was observed, and morphological variations in microglia were detected in both groups (3xTg-AD and NoTg). Additionally, in the brain of the TPP-treated group, some changes in mRNA gene expression were recorded. Together, these findings describe hippocampal microglial and amyloid profiles following TPP treatment in 3xTg-AD mice and provide a basis for further investigation of thiamine-dependent pathways in AD-related neuroinflammatory contexts.

Indexed as

AmyloidHippocampusMicrogliaThiamine PyrophosphateAlzheimer DiseaseAnimalsDisease Models, AnimalFemaleGene Expression ProfilingMiceMice, TransgenicAmyloidThiamine PyrophosphateAlzheimer’s disease treatmentAlzheimer’s geneticsamyloid-β clearancegene expressionmetabolic flexibilitymicroglial morphologymitochondrial dysfunctionneuroinflammationosmotic pumpvitamin B1

Identifiers

PMID42278547
PMCPMC13257033

What OpenQuestion 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 OpenQuestion graph.