Evidence map›Paper›PMID 25705176›Full record

ArticleFrontiers in cellular neuroscience2015

Choroid plexus dysfunction impairs beta-amyloid clearance in a triple transgenic mouse model of Alzheimer's disease.

Ibrahim González-Marrero, Lydia Giménez-Llort, Conrad E Johanson, Emilia María Carmona-Calero, Leandro Castañeyra-Ruiz, José Miguel Brito-Armas, Agustín Castañeyra-Perdomo, Rafael Castro-Fuentes

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cellular neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed
6.8field-weighted citation impact, top 3% of its field
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

81 citing papers in PubMed, 130 citations in OpenAlex.

  1. Review
  2. Chronic kidney disease and cognitive decline: choroid plexus remodeling, glymphatic dysfunction, and alzheimer biomarker interpretation.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026
    Review
  3. Choroid plexus volume in pathology-confirmed Alzheimer's disease.The journal of prevention of Alzheimer's disease · 2026
    Article
  4. Choroid plexus remodeling linked to impaired CSF-mediated clearance and Alzheimer's disease progression.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
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21 more citing papers are in PubMed but not listed here.

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 at 3 institutions in 2 countries.

Ibrahim González-MarreroDepartment of Human Anatomy, School of Medicine, University of La Laguna Tenerife, Spain.
Lydia Giménez-LlortInstitute of Neurosciences and Department of Psychiatry and Forensic Medicine, Autonomous University of Barcelona Barcelona, Spain.
Conrad E JohansonDepartment of Neurosurgery, Alpert Medical School at Brown University Providence, Rhode Island, USA.
Emilia María Carmona-CaleroDepartment of Human Anatomy, School of Medicine, University of La Laguna Tenerife, Spain.
Leandro Castañeyra-RuizDepartment of Human Anatomy, School of Medicine, University of La Laguna Tenerife, Spain.
José Miguel Brito-ArmasDepartment of Physiology, School of Medicine, University of La Laguna Tenerife, Spain.
Agustín Castañeyra-PerdomoDepartment of Human Anatomy, School of Medicine, University of La Laguna Tenerife, Spain.
Rafael Castro-FuentesDepartment of Physiology, School of Medicine, University of La Laguna Tenerife, Spain.
Universidad de La Laguna · ESBrown University · USUniversitat Autònoma de Barcelona · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Compromised secretory function of choroid plexus (CP) and defective cerebrospinal fluid (CSF) production, along with accumulation of beta-amyloid (Aβ) peptides at the blood-CSF barrier (BCSFB), contribute to complications of Alzheimer's disease (AD). The AD triple transgenic mouse model (3xTg-AD) at 16 month-old mimics critical hallmarks of the human disease: β-amyloid (Aβ) plaques and neurofibrillary tangles (NFT) with a temporal- and regional- specific profile. Currently, little is known about transport and metabolic responses by CP to the disrupted homeostasis of CNS Aβ in AD. This study analyzed the effects of highly-expressed AD-linked human transgenes (APP, PS1 and tau) on lateral ventricle CP function. Confocal imaging and immunohistochemistry revealed an increase only of Aβ42 isoform in epithelial cytosol and in stroma surrounding choroidal capillaries; this buildup may reflect insufficient clearance transport from CSF to blood. Still, there was increased expression, presumably compensatory, of the choroidal Aβ transporters: the low density lipoprotein receptor-related protein 1 (LRP1) and the receptor for advanced glycation end product (RAGE). A thickening of the epithelial basal membrane and greater collagen-IV deposition occurred around capillaries in CP, probably curtailing solute exchanges. Moreover, there was attenuated expression of epithelial aquaporin-1 and transthyretin (TTR) protein compared to Non-Tg mice. Collectively these findings indicate CP dysfunction hypothetically linked to increasing Aβ burden resulting in less efficient ion transport, concurrently with reduced production of CSF (less sink action on brain Aβ) and diminished secretion of TTR (less neuroprotection against cortical Aβ toxicity). The putative effects of a disabled CP-CSF system on CNS functions are discussed in the context of AD.

Indexed as

3xTg-AD miceAlzheimer diseaseamyloid-βaquaporin-1choroid plexuscollagen-IVdysfunctiontransthyretin

Identifiers

PMID25705176
PMCPMC4319477
OpenAlexW2038214340

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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.