Evidence map›Paper›PMID 35630602›Full record

ArticleMolecules (Basel, Switzerland)2022

The Reversible Carnitine Palmitoyltransferase 1 Inhibitor (Teglicar) Ameliorates the Neurodegenerative Phenotype in a Drosophila Huntington's Disease Model by Acting on the Expression of Carnitine-Related Genes.

Carla Bertapelle, Maria Rosaria Carillo, Nunzio Antonio Cacciola, Yulii V Shidlovskii, Gianfranco Peluso, Filomena Anna Digilio

Open access · goldAbstract read
In one paragraph

Article in Molecules (Basel, Switzerland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.4field-weighted citation impact, top 48% 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

5 citing papers in PubMed, 6 citations in OpenAlex.

  1. Nuclear MBL-1 modulates mitochondrial morphology through carnitine palmitoyltransferase inProceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  2. Review
  3. Decoding Nucleotide Repeat Expansion Diseases: Novel Insights fromInternational journal of molecular sciences · 2024
    Review
  4. Review
  5. 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

6 authors at 3 institutions in 2 countries.

Carla BertapelleResearch Institute on Terrestrial Ecosystems (IRET), UOS Naples-CNR, Via Pietro Castellino 111, 80131 Naples, Italy.
Maria Rosaria CarilloResearch Institute on Terrestrial Ecosystems (IRET), UOS Naples-CNR, Via Pietro Castellino 111, 80131 Naples, Italy.
Nunzio Antonio CacciolaResearch Institute on Terrestrial Ecosystems (IRET), UOS Naples-CNR, Via Pietro Castellino 111, 80131 Naples, Italy.ORCID 0000-0002-0780-9844
Yulii V ShidlovskiiDepartment of Gene Expression Regulation in Development, Institute of Gene Biology, Russian Academy of Sciences, 34/5 Vavilov St., 119334 Moscow, Russia.ORCID 0000-0002-3643-9889
Gianfranco PelusoResearch Institute on Terrestrial Ecosystems (IRET), UOS Naples-CNR, Via Pietro Castellino 111, 80131 Naples, Italy.
Filomena Anna DigilioResearch Institute on Terrestrial Ecosystems (IRET), UOS Naples-CNR, Via Pietro Castellino 111, 80131 Naples, Italy.ORCID 0000-0002-9342-3760
University of Naples Federico II · ITSechenov University · RUUniversity of Campania "Luigi Vanvitelli" · IT

Funding

National Research Council 0010655/2021Russian Foundation for Basic Research 20-54-7803
6 · The paper itself

Abstract

Huntington's disease (HD) is a dramatic neurodegenerative disorder caused by the abnormal expansion of a CAG triplet in the huntingtin gene, producing an abnormal protein. As it leads to the death of neurons in the cerebral cortex, the patients primarily present with neurological symptoms, but recently metabolic changes resulting from mitochondrial dysfunction have been identified as novel pathological features. The carnitine shuttle is a complex consisting of three enzymes whose function is to transport the long-chain fatty acids into the mitochondria. Here, its pharmacological modification was used to test the hypothesis that shifting metabolism to lipid oxidation exacerbates the HD symptoms. Behavioural and transcriptional analyses were carried out on HD Drosophila model, to evaluate the involvement of the carnitine cycle in this pathogenesis. Pharmacological inhibition of

Indexed as

CarnitineCarnitine O-PalmitoyltransferaseHuntington DiseaseAnimalsDisease Models, AnimalDrosophilaPhenotypeCarnitineCarnitine O-Palmitoyltransferasecarnitine shuttleDrosophila melanogasterHuntington’s diseaseL-carnitinemitochondrianeurodegenerationβ-oxidation

Identifiers

PMID35630602
PMCPMC9146098
OpenAlexW4280565578

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.