Evidence map›Paper›PMID 42204549›Full record

ArticleCell communication and signaling : CCS2026

Visceral adipose tissue differentially affects tau and Aβ pathology in 3xTg-AD mice.

Laura Trujillo-Estrada, Miriam Bettinetti-Luque, Juana Andreo-Lopez, Celia da Cunha, Mario Morales-Cabello, Cynthia Campos-Moreno, Elisabeth Sanchez-Mejias, Stefania Forner, Alessandra C Martini, Raquel Sanchez-Varo and 3 more

Abstract read
In one paragraph

Article in Cell communication and signaling : CCS, 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

13 authors.

Laura Trujillo-EstradaInstitute for Memory Impairments and Neurological Disorders, University of California, Irvine, CA, 92697, USA.
Miriam Bettinetti-LuqueDepartamento Biologia Celular, Genetica y Fisiologia, Instituto de Investigacion Biomedica de Malaga IBIMA-Plataforma Bionand, Facultad de Ciencias, Universidad de Malaga, Malaga, Spain.
Juana Andreo-LopezDepartamento Biologia Celular, Genetica y Fisiologia, Instituto de Investigacion Biomedica de Malaga IBIMA-Plataforma Bionand, Facultad de Ciencias, Universidad de Malaga, Malaga, Spain.
Celia da CunhaInstitute for Memory Impairments and Neurological Disorders, University of California, Irvine, CA, 92697, USA.
Mario Morales-CabelloDepartamento Biologia Celular, Genetica y Fisiologia, Instituto de Investigacion Biomedica de Malaga IBIMA-Plataforma Bionand, Facultad de Ciencias, Universidad de Malaga, Malaga, Spain.
Cynthia Campos-MorenoDepartamento Biologia Celular, Genetica y Fisiologia, Instituto de Investigacion Biomedica de Malaga IBIMA-Plataforma Bionand, Facultad de Ciencias, Universidad de Malaga, Malaga, Spain.
Elisabeth Sanchez-MejiasDepartamento Biologia Celular, Genetica y Fisiologia, Instituto de Investigacion Biomedica de Malaga IBIMA-Plataforma Bionand, Facultad de Ciencias, Universidad de Malaga, Malaga, Spain.
Stefania FornerInstitute for Memory Impairments and Neurological Disorders, University of California, Irvine, CA, 92697, USA.
Alessandra C MartiniInstitute for Memory Impairments and Neurological Disorders, University of California, Irvine, CA, 92697, USA.
Raquel Sanchez-VaroDepartamento Biologia Celular, Genetica y Fisiologia, Instituto de Investigacion Biomedica de Malaga IBIMA-Plataforma Bionand, Facultad de Ciencias, Universidad de Malaga, Malaga, Spain.
Antonia GutierrezDepartamento Biologia Celular, Genetica y Fisiologia, Instituto de Investigacion Biomedica de Malaga IBIMA-Plataforma Bionand, Facultad de Ciencias, Universidad de Malaga, Malaga, Spain.
Frank M LaFerlaInstitute for Memory Impairments and Neurological Disorders, University of California, Irvine, CA, 92697, USA. laferla@uci.edu.
David Baglietto-VargasInstitute for Memory Impairments and Neurological Disorders, University of California, Irvine, CA, 92697, USA. d.baglietto@uma.es.

Funding

UC Irvine MODEL-ADU54AG054349 · NIA · UNIVERSITY OF CALIFORNIA-IRVINE · PI Kim Green, FRANK M LAFERLA · 2017 to 2026
$71.9M
Alzheimer's Association AARG-22-928219BrightFocus Foundation A2015535SIBIMA Plataforma Bionand INTAR25-11Instituto de Salud Carlos III PI21/00915Ministerio de Ciencia e Innovación PID2019-108911RA-100Ministerio de Ciencia e Innovación, programa Beatriz Galindo BEAGAL18/00052NIA NIH HHS U54 AG054349NIH HHS U54-AG054349Universidad de Málaga 961.662University of Malaga, Spain B1-2021_32
6 · The paper itself

Abstract

backgroundAlzheimer's disease (AD) is a complex disorder involving multiple cellular and molecular mechanisms. Recent evidence suggests that metabolic alterations play a crucial role in AD progression. Likewise, diabetes and obesity-two major metabolic diseases-are well-established risk factors for AD. These conditions are associated with a significant expansion of white adipose tissue (WAT). Here, we hypothesize that visceral WAT may act as a key mediator between peripheral metabolic dysfunction and brain illnesses.

methodsImmunohistochemistry and biochemical approaches were used to evaluate the WAT from WT and db/db mice. Similar techniques were applied to examine the brain tissue of 3xTg-AD mice that received white epididymal fat pads from WT or db/db donors and determine the impact of adipose tissue transplantation on tau and Aβ pathology.

resultsOur study revealed that recipient 3xTg-AD mice that received db/db fat pads developed profound changes in tau pathology due to increased expression of the cyclin-dependent kinase 5 activator p25 compared with 3xTg-AD mice that received fad pads from WT or sham mice. This increment in p25/cdk5 was associated with a prominent inflammatory response induced by the WAT transplant. Moreover, the opposite effect on Aβ pathology was found. The reduction in Aβ levels was correlated with an increase in microglial phagocytic capacity.

conclusionsOverall, our study demonstrated a novel crosstalk between AD and metabolic disorders through white adipose signaling resulting in differential effects on tau and Aβ pathology mediated by an activated immune response.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesIntra-Abdominal Fattau ProteinsAdipose Tissue, WhiteAnimalsBrainCyclin-Dependent Kinase 5MaleMiceMice, Inbred C57BLMice, TransgenicAmyloid beta-PeptidesCyclin-Dependent Kinase 5tau ProteinsAlzheimer’s diseaseAβInflammationObesityTauWhite adipose tissue

Identifiers

PMID42204549
PMCPMC13404139

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LicenceCC BY-NC-ND
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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.