Evidence map›Paper›PMID 28475111›Full record

ReviewJournal of clinical medicine2017

Riboflavin Responsive Mitochondrial Dysfunction in Neurodegenerative Diseases.

Tamilarasan Udhayabanu, Andreea Manole, Mohan Rajeshwari, Perumal Varalakshmi, Henry Houlden, Balasubramaniem Ashokkumar

Open access · goldAbstract readReview
In one paragraph

Review in Journal of clinical medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed, 1 pooled it
6.2field-weighted citation impact, top 3% 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

61 citing papers in PubMed, 1 synthesis or guideline pooled it, 117 citations in OpenAlex.

  1. Emerging perspectives on mitochondrial dysfunctioning and inflammation in epileptogenesis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2021
    Pooled it
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  11. B Vitamins and Ocular Health.Clinical ophthalmology (Auckland, N.Z.) · 2026
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1 more citing papers are in PubMed but not listed here.

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 2 institutions in 2 countries.

Tamilarasan UdhayabanuDepartment of Genetic Engineering, School of Biotechnology, Madurai Kamaraj University, Madurai 625021, India. udhaya13banu@gmail.com.
Andreea ManoleDepartment of Molecular Neuroscience and Neurogenetics Laboratory, UCL Institute of Neurology, Queen Square, London WC1N 3BG, UK. andreea.manole.13@ucl.ac.uk.
Mohan RajeshwariDepartment of Genetic Engineering, School of Biotechnology, Madurai Kamaraj University, Madurai 625021, India. ponderofbiotech@gmail.com.
Perumal VaralakshmiDepartment of Molecular Microbiology, School of Biotechnology, Madurai Kamaraj University, Madurai 625021, India. vara5277@gmail.com.
Henry HouldenDepartment of Molecular Neuroscience and Neurogenetics Laboratory, UCL Institute of Neurology, Queen Square, London WC1N 3BG, UK. h.houlden@ucl.ac.uk.
Balasubramaniem AshokkumarDepartment of Genetic Engineering, School of Biotechnology, Madurai Kamaraj University, Madurai 625021, India. rbashokkumar@yahoo.com.
Madurai Kamaraj University · INNational Hospital for Neurology and Neurosurgery · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondria are the repository for various metabolites involved in diverse energy-generating processes, like the TCA cycle, oxidative phosphorylation, and metabolism of amino acids, fatty acids, and nucleotides, which rely significantly on flavoenzymes, such as oxidases, reductases, and dehydrogenases. Flavoenzymes are functionally dependent on biologically active flavin adenine dinucleotide (FAD) or flavin mononucleotide (FMN), which are derived from the dietary component riboflavin, a water soluble vitamin. Riboflavin regulates the structure and function of flavoenzymes through its cofactors FMN and FAD and, thus, protects the cells from oxidative stress and apoptosis. Hence, it is not surprising that any disturbance in riboflavin metabolism and absorption of this vitamin may have consequences on cellular FAD and FMN levels, resulting in mitochondrial dysfunction by reduced energy levels, leading to riboflavin associated disorders, like cataracts, neurodegenerative and cardiovascular diseases, etc. Furthermore, mutations in either nuclear or mitochondrial DNA encoding for flavoenzymes and flavin transporters significantly contribute to the development of various neurological disorders. Moreover, recent studies have evidenced that riboflavin supplementation remarkably improved the clinical symptoms, as well as the biochemical abnormalities, in patients with neuronopathies, like Brown-Vialetto-Van-Laere syndrome (BVVLS) and Fazio-Londe disease. This review presents an updated outlook on the cellular and molecular mechanisms of neurodegenerative disorders in which riboflavin deficiency leads to dysfunction in mitochondrial energy metabolism, and also highlights the significance of riboflavin supplementation in aforementioned disease conditions. Thus, the outcome of this critical assessment may exemplify a new avenue to enhance the understanding of possible mechanisms in the progression of neurodegenerative diseases and may provide new rational approaches of disease surveillance and treatment.

Indexed as

BVVLSFADFMNmitochondrial dysfunctionmotor neuronopathyriboflavin

Identifiers

PMID28475111
PMCPMC5447943
OpenAlexW2610637726

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.