Evidence map›Paper›PMID 33580102›Full record

ArticleScientific reports2021

High levels of 27-hydroxycholesterol results in synaptic plasticity alterations in the hippocampus.

Raul Loera-Valencia, Erika Vazquez-Juarez, Alberto Muñoz, Gorka Gerenu, Marta Gómez-Galán, Maria Lindskog, Javier DeFelipe, Angel Cedazo-Minguez, Paula Merino-Serrais

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
5.2field-weighted citation impact, top 4% 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

26 citing papers in PubMed, 37 citations in OpenAlex.

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  4. Emerging Roles of Bile Acids in Neuroinflammation.International journal of molecular sciences · 2025
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  13. Article
  14. Oxysterols in Central and Peripheral Synaptic Communication.Advances in experimental medicine and biology · 2024
    Article
  15. Article
  16. Review
  17. Review
  18. Article
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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

9 authors at 4 institutions in 2 countries.

Raul Loera-ValenciaDepartment of Neurobiology, Care Sciences and Society, Division of Neurogeriatrics, Center for Alzheimer Research, Karolinska Institutet, Stockholm, Sweden.
Erika Vazquez-JuarezDepartment of Neurobiology, Care Sciences and Society, Division of Neurogeriatrics, Center for Alzheimer Research, Karolinska Institutet, Stockholm, Sweden.
Alberto MuñozInstituto Cajal (CSIC), Avenida Doctor Arce 37, 28002, Madrid, Spain.
Gorka GerenuDepartment of Neurobiology, Care Sciences and Society, Division of Neurogeriatrics, Center for Alzheimer Research, Karolinska Institutet, Stockholm, Sweden.
Marta Gómez-GalánDepartment of Physiology and Pharmacology, Section for Anesthesiology and Intensive Care Medicine, Karolinska Institutet, Stockholm, Sweden.
Maria LindskogDepartment of Neurobiology, Care Sciences and Society, Division of Neurogeriatrics, Center for Alzheimer Research, Karolinska Institutet, Stockholm, Sweden.
Javier DeFelipeInstituto Cajal (CSIC), Avenida Doctor Arce 37, 28002, Madrid, Spain.
Angel Cedazo-MinguezDepartment of Neurobiology, Care Sciences and Society, Division of Neurogeriatrics, Center for Alzheimer Research, Karolinska Institutet, Stockholm, Sweden. angel.cedazo-minguez@ki.se.
Paula Merino-SerraisDepartment of Neurobiology, Care Sciences and Society, Division of Neurogeriatrics, Center for Alzheimer Research, Karolinska Institutet, Stockholm, Sweden. paula.merino-serrais@cajal.csic.es.
Karolinska Institutet · SEInstituto Cajal · ESBiogipuzkoa Health Research Institute · ESUniversidad Complutense de Madrid · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alterations in brain cholesterol homeostasis in midlife are correlated with a higher risk of developing Alzheimer's disease (AD). However, global cholesterol-lowering therapies have yielded mixed results when it comes to slowing down or preventing cognitive decline in AD. We used the transgenic mouse model Cyp27Tg, with systemically high levels of 27-hydroxycholesterol (27-OH) to examine long-term potentiation (LTP) in the hippocampal CA1 region, combined with dendritic spine reconstruction of CA1 pyramidal neurons to detect morphological and functional synaptic alterations induced by 27-OH high levels. Our results show that elevated 27-OH levels lead to enhanced LTP in the Schaffer collateral-CA1 synapses. This increase is correlated with abnormally large dendritic spines in the stratum radiatum. Using immunohistochemistry for synaptopodin (actin-binding protein involved in the recruitment of the spine apparatus), we found a significantly higher density of synaptopodin-positive puncta in CA1 in Cyp27Tg mice. We hypothesize that high 27-OH levels alter synaptic potentiation and could lead to dysfunction of fine-tuned processing of information in hippocampal circuits resulting in cognitive impairment. We suggest that these alterations could be detrimental for synaptic function and cognition later in life, representing a potential mechanism by which hypercholesterolemia could lead to alterations in memory function in neurodegenerative diseases.

Indexed as

Alzheimer DiseaseAnimalsCA1 Region, HippocampalCognitive DysfunctionDendritic SpinesDisease Models, AnimalHippocampusHumansHydroxycholesterolsLong-Term PotentiationMaleMiceMice, TransgenicMicrofilament ProteinsNeuronal PlasticityPyramidal Cells27-hydroxycholesterolHydroxycholesterolsMicrofilament ProteinsSynpo protein, mouse

Identifiers

PMID33580102
PMCPMC7881004
OpenAlexW3129113626

What OpenQuestion holds

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LicenceCC BY
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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.