Evidence map›Paper›PMID 32276655›Full record

ArticleBMC research notes2020

The cholesterol 24-hydroxylase activates autophagy and decreases mutant huntingtin build-up in a neuroblastoma culture model of Huntington's disease.

Clévio Nóbrega, André Conceição, Rafael G Costa, Rebekah Koppenol, Raquel L Sequeira, Ricardo Nunes, Sara Carmo-Silva, Adriana Marcelo, Carlos A Matos, Sandrine Betuing and 3 more

Open access · goldAbstract read
In one paragraph

Article in BMC research notes, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.2field-weighted citation impact, top 24% 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

9 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Altered Cholesterol Homeostasis in Huntington's Disease.Frontiers in aging neuroscience · 2022
    Review
  7. Review
  8. Article
  9. 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

13 authors at 6 institutions in 2 countries.

Clévio NóbregaDepartment of Biomedical Sciences and Medicine, Universidade do Algarve, Faro, Portugal. cdnobrega@ualg.pt.
André ConceiçãoCentre for Biomedical Research, Universidade do Algarve, Faro, Portugal.
Rafael G CostaDepartment of Biomedical Sciences and Medicine, Universidade do Algarve, Faro, Portugal.
Rebekah KoppenolDepartment of Biomedical Sciences and Medicine, Universidade do Algarve, Faro, Portugal.
Raquel L SequeiraDepartment of Biomedical Sciences and Medicine, Universidade do Algarve, Faro, Portugal.
Ricardo NunesDepartment of Biomedical Sciences and Medicine, Universidade do Algarve, Faro, Portugal.
Sara Carmo-SilvaCenter for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal.
Adriana MarceloDepartment of Biomedical Sciences and Medicine, Universidade do Algarve, Faro, Portugal.
Carlos A MatosDepartment of Biomedical Sciences and Medicine, Universidade do Algarve, Faro, Portugal.
Sandrine BetuingNeuronal Signaling and Gene Regulation, Neurosciences Paris Seine, Institut de Biologie Paris Seine, Sorbonne Université, Faculté des Sciences et Ingénerie, INSERM/UMR-S 1130, CNRS/UMR 8246, 75005, Paris, France.
Jocelyne CabocheNeuronal Signaling and Gene Regulation, Neurosciences Paris Seine, Institut de Biologie Paris Seine, Sorbonne Université, Faculté des Sciences et Ingénerie, INSERM/UMR-S 1130, CNRS/UMR 8246, 75005, Paris, France.
Nathalie CartierINSERM U1127, Institut du Cerveau et de la Moelle épinière (ICM), Hôpital Pitié-Salpêtrière, 47 bd de l'Hôpital, 75013, Paris, France. nathalie.cartier@inserm.fr.
Sandro AlvesBrainvectis, Institut du Cerveau et de la Moelle épinière (ICM), Hôpital Pitié-Salpêtrière, 47 boulevard de l'Hôpital Paris, 75646, Paris Cedex 13, France. sandropfalves@gmail.com.
Algarve Biomedical Center · PTUniversity of Algarve · PTInstitut du Cerveau · FRInserm · FRInstitut de Biologie Paris-Seine · FRUniversity of Coimbra · PT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveCompromised brain cholesterol turnover and altered regulation of brain cholesterol metabolism have been allied with some neurodegenerative diseases, including Huntington's disease (HD). Following our previous studies in HD, in this study we aim to investigate in vitro in a neuroblastoma cellular model of HD, the effect of CYP46A1 overexpression, an essential enzyme in cholesterol metabolism, on huntingtin aggregation and levels.

resultsWe found that CYP46A1 reduces the quantity and size of mutant huntingtin aggregates in cells, as well as the levels of mutant huntingtin protein. Additionally, our results suggest that the observed beneficial effects of CYP46A1 in HD cells are linked to the activation of autophagy. Taken together, our results further demonstrate that CYP46A1 is a pertinent target to counteract HD progression.

Indexed as

AutophagyNeuroblastomaAnimalsCell Line, TumorCells, CulturedCholesterol 24-HydroxylaseHuntingtin ProteinHuntington DiseaseMiceMutant ProteinsCholesterol 24-HydroxylaseHuntingtin ProteinMutant ProteinsAutophagyCholesterolCYP46A1HuntingtinNeuroblastoma cells

Identifiers

PMID32276655
PMCPMC7149904
OpenAlexW3015376006

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.