Evidence mapPaperPMID 40537787Full record

ArticleJournal of neuroinflammation2025

KChIP3 fosters neuroinflammation and synaptic dysfunction in the 5XFAD mouse model of Alzheimer's disease.

Bolivar Arcos-Encarnación, Eladio Cortes-Flores, Isabel Barón-Mendoza, Jorge Luis Almazán, David Valle-García, Sol Díaz de León-Guerrero, Ladislav Hovan, Karla F Meza-Sosa, Nohemi Camacho-Concha, Jeovanis Gil and 5 more

Abstract read
In one paragraph

Article in Journal of neuroinflammation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. Article
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

15 authors.

Bolivar Arcos-Encarnación *Laboratorio de Neuroinmunobiología, Departamento de Medicina Molecular y Bioprocesos, Instituto de Biotecnología, Universidad Nacional Autónoma de México (UNAM), 62210, Cuernavaca, Morelos, México.
Eladio Cortes-Flores *Laboratorio de Neuroinmunobiología, Departamento de Medicina Molecular y Bioprocesos, Instituto de Biotecnología, Universidad Nacional Autónoma de México (UNAM), 62210, Cuernavaca, Morelos, México.
Isabel Barón-MendozaDepartamento de Medicina Genómica y Toxicología Ambiental, Instituto de Investigaciones Biomédicas, UNAM, 04510, Ciudad de Mexico, México.
Jorge Luis AlmazánLaboratorio de Neuroinmunobiología, Departamento de Medicina Molecular y Bioprocesos, Instituto de Biotecnología, Universidad Nacional Autónoma de México (UNAM), 62210, Cuernavaca, Morelos, México.
David Valle-GarcíaLaboratorio de Neuroinmunobiología, Departamento de Medicina Molecular y Bioprocesos, Instituto de Biotecnología, Universidad Nacional Autónoma de México (UNAM), 62210, Cuernavaca, Morelos, México.
Sol Díaz de León-GuerreroLaboratorio de Neuroinmunobiología, Departamento de Medicina Molecular y Bioprocesos, Instituto de Biotecnología, Universidad Nacional Autónoma de México (UNAM), 62210, Cuernavaca, Morelos, México.
Ladislav HovanNorwegian Centre for Molecular Biosciences and Medicine (NCMBM), Nordic EMBL Partnership, University of Oslo, Gaustadalléen 21, 0318, Oslo, Norway.
Karla F Meza-SosaLaboratorio de Neuroinmunobiología, Departamento de Medicina Molecular y Bioprocesos, Instituto de Biotecnología, Universidad Nacional Autónoma de México (UNAM), 62210, Cuernavaca, Morelos, México.
Nohemi Camacho-ConchaLaboratorio de Neuroinmunobiología, Departamento de Medicina Molecular y Bioprocesos, Instituto de Biotecnología, Universidad Nacional Autónoma de México (UNAM), 62210, Cuernavaca, Morelos, México.
Jeovanis GilClinical Chemistry Section, Department of Translational Medicine, Lund University, 22242 Lund, Sweden.
Marieke Lydia KuijjerNorwegian Centre for Molecular Biosciences and Medicine (NCMBM), Nordic EMBL Partnership, University of Oslo, Gaustadalléen 21, 0318, Oslo, Norway.
Aliesha González-ArenasDepartamento de Medicina Genómica y Toxicología Ambiental, Instituto de Investigaciones Biomédicas, UNAM, 04510, Ciudad de Mexico, México.
Sergio Encarnación-GuevaraLaboratorio de Proteómica, Centro de Ciencias Genómicas UNAM, 62210, Cuernavaca, Morelos, México.
Gustavo Pedraza-AlvaLaboratorio de Neuroinmunobiología, Departamento de Medicina Molecular y Bioprocesos, Instituto de Biotecnología, Universidad Nacional Autónoma de México (UNAM), 62210, Cuernavaca, Morelos, México.
Leonor Pérez-MartínezLaboratorio de Neuroinmunobiología, Departamento de Medicina Molecular y Bioprocesos, Instituto de Biotecnología, Universidad Nacional Autónoma de México (UNAM), 62210, Cuernavaca, Morelos, México. leonor.perez@ibt.unam.mx.

Funding

Consejo Nacional de Humanidades, Ciencias y Tecnologías, México CF/2019-40792Consejo Nacional de Humanidades, Ciencias y Tecnologías, México CONAHCYT 425859Consejo Nacional de Humanidades, Ciencias y Tecnologías, México IFC 2016-2282Consejo Nacional de Humanidades, Ciencias y Tecnologías, México, CONAHCYT CBF2023-2024-878Dirección General de Asuntos del Personal Académico, Universidad Nacional Autónoma de México IN213522Dirección General de Asuntos del Personal Académico, Universidad Nacional Autónoma de México IN216922Dirección General de Asuntos del Personal Académico, Universidad Nacional Autónoma de México IN217822
6 · The paper itself

Abstract

Alzheimer's disease (AD) is a progressive neurodegenerative disorder marked by β-amyloid (βA) accumulation, neuroinflammation, excessive synaptic pruning, and cognitive decline. Despite extensive research, effective treatments remain elusive. Here, we identify potassium channel-interacting protein 3 (KChIP3) as a key driver of AD pathology using the 5XFAD mouse model. KChIP3 levels were significantly elevated in the hippocampus of 5XFAD mice, correlating with βA burden and neuroinflammation. This upregulation was triggered by inflammatory signaling via the NLRP3 inflammasome and Caspase-1 activation. Notably, genetic deletion of KChIP3 (5XFAD/KChIP3

Indexed as

Alzheimer DiseaseKv Channel-Interacting ProteinsNeuroinflammatory DiseasesSynapsesAmyloid beta-PeptidesAnimalsDisease Models, AnimalHippocampusMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicAmyloid beta-PeptidesKv Channel-Interacting Proteins5XFAD miceAgingAlzheimer’s diseaseKChIP3LearningLTPMemoryMicrogliaNeuroinflammationSynaptic plasticity

Identifiers

PMID40537787
PMCPMC12178027

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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.