Evidence map›Paper›PMID 34440878›Full record

ArticleCells2021

The Neuroprotective Effect of L-Carnitine against Glyceraldehyde-Induced Metabolic Impairment: Possible Implications in Alzheimer's Disease.

Simona Magi, Alessandra Preziuso, Silvia Piccirillo, Francesca Giampieri, Danila Cianciosi, Monia Orciani, Salvatore Amoroso

Open access · goldAbstract read
In one paragraph

Article in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

17 citing papers in PubMed, 30 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Article
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  7. Review
  8. Food science & nutrition · 2025
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  9. Review
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  11. Article
  12. Review
  13. Review
  14. A new KCell death discovery · 2022
    Article
  15. Review
  16. Review
  17. Taurine Stabilizing Effect on Lysozyme.Life (Basel, Switzerland) · 2022
    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

7 authors at 1 institution in 2 countries.

Simona MagiDepartment of Biomedical Sciences and Public Health, School of Medicine, University "Politecnica delle Marche", Via Tronto 10/A, 60126 Ancona, Italy.
Alessandra PreziusoDepartment of Biomedical Sciences and Public Health, School of Medicine, University "Politecnica delle Marche", Via Tronto 10/A, 60126 Ancona, Italy.ORCID 0000-0001-9721-2023
Silvia PiccirilloDepartment of Biomedical Sciences and Public Health, School of Medicine, University "Politecnica delle Marche", Via Tronto 10/A, 60126 Ancona, Italy.
Francesca GiampieriDepartment of Clinical Sciences, School of Medicine, University "Politecnica delle Marche", Via Tronto 10/A, 60126 Ancona, Italy.ORCID 0000-0002-8151-9132
Danila CianciosiDepartment of Clinical Sciences, School of Medicine, University "Politecnica delle Marche", Via Tronto 10/A, 60126 Ancona, Italy.
Monia OrcianiDepartment of Clinical and Molecular Sciences-Histology, School of Medicine, University "Politecnica delle Marche", Via Tronto 10/A, 60126 Ancona, Italy.ORCID 0000-0003-4503-3693
Salvatore AmorosoDepartment of Biomedical Sciences and Public Health, School of Medicine, University "Politecnica delle Marche", Via Tronto 10/A, 60126 Ancona, Italy.
Marche Polytechnic University · IT

Funding

Ministero dell'Istruzione, dell'Università e della Ricerca 2017YH3SXK
6 · The paper itself

Abstract

Alzheimer's disease (AD) is a neurodegenerative disorder characterized by progressive cognitive regression and memory loss. Dysfunctions of both glucose metabolism and mitochondrial dynamics have been recognized as the main upstream events of the degenerative processes leading to AD. It has been recently found that correcting cell metabolism by providing alternative substrates can prevent neuronal injury by retaining mitochondrial function and reducing AD marker levels. Here, we induced an AD-like phenotype by using the glycolysis inhibitor glyceraldehyde (GA) and explored whether L-carnitine (4-N-trimethylamino-3-hydroxybutyric acid, LC) could mitigate neuronal damage, both in SH-SY5Y neuroblastoma cells and in rat primary cortical neurons. We have already reported that GA significantly modified AD marker levels; here we demonstrated that GA dramatically compromised cellular bioenergetic status, as revealed by glycolysis and oxygen consumption rate (OCR) evaluation. We found that LC ameliorated cell survival, improved OCR and ATP synthesis, prevented the loss of the mitochondrial membrane potential (Δψ

Indexed as

Adenosine TriphosphateAlzheimer DiseaseAnimalsCarnitineCell SurvivalGlyceraldehydeGlycolysisHumansMembrane Potential, MitochondrialMitochondriaModels, BiologicalNeuronsNeuroprotective AgentsOxygen ConsumptionPhosphorylationRatsAdenosine TriphosphateCarnitineGlyceraldehydeMAPT protein, humanNeuroprotective AgentsReactive Oxygen Speciestau ProteinsAlzheimer’s diseaseL-carnitinemetabolic dysfunctionsmitochondrial membrane potentialneuronal survivaloxidative stressoxygen consumption rateTau hyperphosphorylation

Identifiers

PMID34440878
PMCPMC8394427
OpenAlexW3195097643

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.