Evidence map›Paper›PMID 34164711›Full record

ArticleArchives of toxicology2021

Mechanistic perspectives on differential mitochondrial-based neuroprotective effects of several carnitine forms in Alzheimer's disease in vitro model.

Sandra I Mota, Inês Pita, Rodolfo Águas, Slah Tagorti, Ashraf Virmani, Frederico C Pereira, A Cristina Rego

Registry-linked trialAbstract readComparative Study
PubMed Publisher
In one paragraph

Article in Archives of toxicology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT01320527 (A Phase II Clinical Trial of a Vitamin/Nutriceutical Formulation for Alzheimer's Disease), which is not on this map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
–field-weighted citation impact
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.

NCT01320527 phase2completednot on this map

A Phase II Clinical Trial of a Vitamin/Nutriceutical Formulation for Alzheimer's Disease

TypeinterventionalSponsorUniversity of Massachusetts, WorcesterRan2008 to 2012Enrolled135ConditionsAlzheimer's Disease, Mild Cognitive ImpairmentArmsNutriceutical formulation, Placebo
3 · Its place in the literature

Who cites it

15 citing papers in PubMed.

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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

7 authors.

Sandra I MotaCNC-Center for Neuroscience and Cell Biology, CIBB - Centre for Innovative Biomedicine and Biotechnology, University of Coimbra, 3004-504, Coimbra, Portugal.ORCID http://orcid.org/0000-0001-9623-5012
Inês PitaInstitute of Pharmacology and Experimental Therapeutics, Faculty of Medicine, University of Coimbra, 3004-504, Coimbra, Portugal.ORCID http://orcid.org/0000-0002-6310-4048
Rodolfo ÁguasCNC-Center for Neuroscience and Cell Biology, CIBB - Centre for Innovative Biomedicine and Biotechnology, University of Coimbra, 3004-504, Coimbra, Portugal.
Slah TagortiAlfasigma B.V, 3528 BG, Utrecht, The Netherlands.
Ashraf VirmaniAlfasigma B.V, 3528 BG, Utrecht, The Netherlands.ORCID http://orcid.org/0000-0003-1216-6393
Frederico C PereiraInstitute of Pharmacology and Experimental Therapeutics, Faculty of Medicine, University of Coimbra, 3004-504, Coimbra, Portugal. fredcp@ci.uc.pt.ORCID http://orcid.org/0000-0002-9381-3320
A Cristina RegoCNC-Center for Neuroscience and Cell Biology, CIBB - Centre for Innovative Biomedicine and Biotechnology, University of Coimbra, 3004-504, Coimbra, Portugal. a.cristina.rego@gmail.com.ORCID http://orcid.org/0000-0003-0700-3776

Funding

AlfaSigma BV PharmaceuticalEuropean Regional Development Fund CENTRO-01-0145-FEDER-000012-HealthyAging2020
6 · The paper itself

Abstract

Mitochondrial deregulation has emerged as one of the earliest pathological events in Alzheimer's disease (AD), the most common age-related neurodegenerative disorder. Improvement of mitochondrial function in AD has been considered a relevant therapeutic approach. L-carnitine (LC), an amino acid derivative involved in the transport of long-chain fatty acids into mitochondria, was previously demonstrated to improve mitochondrial function, having beneficial effects in neurological disorders; moreover, acetyl-L-carnitine (ALC) is currently under phase 4 clinical trial for AD (ClinicalTrials.gov NCT01320527). Thus, in the present study, we investigated the impact of different forms of carnitines, namely LC, ALC and propionyl-L-carnitine (PLC) on mitochondrial toxicity induced by amyloid-beta peptide 1-42 oligomers (AβO; 1 μM) in mature rat hippocampal neurons. Our results indicate that 5 mM LC, ALC and PLC totally rescued the mitochondrial membrane potential and alleviated both the decrease in oxygen consumption rates and the increase in mitochondrial fragmentation induced by AβO. These could contribute to the prevention of neuronal death by apoptosis. Moreover, only ALC ameliorated AβO-evoked changes in mitochondrial movement by reducing the number of stationary mitochondria and promoting reversal mitochondrial movement. Data suggest that carnitines (LC, ALC and PLC) may act differentially to counteract changes in mitochondrial function and movement in neurons subjected to AβO, thus counteracting AD-related pathological phenotypes.

Indexed as

AcetylcarnitineAlzheimer DiseaseAnimalsApoptosisCarnitineCells, CulturedFemaleHippocampusMembrane Potential, MitochondrialMitochondriaNeuronsNeuroprotective AgentsOxygen ConsumptionRatsRats, WistarAcetylcarnitineCarnitineNeuroprotective AgentspropionylcarnitineAcetyl-L-carnitineAlzheimer’s diseaseAmyloid beta peptide oligomersL-CarnitineMitochondrial dysfunctionMitochondrial membrane potentialNeuritic mitochondrial movementOxygen consumption ratePropionyl-L-carnitine

Identifiers

PMID34164711

What OpenQuestion holds

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Registered trials

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.