Evidence map›Paper›PMID 24058333›Full record

ArticleFrontiers in cellular neuroscience2013

A new in vivo model of pantothenate kinase-associated neurodegeneration reveals a surprising role for transcriptional regulation in pathogenesis.

Varun Pandey, Pandey Varun, Hagit Turm, Turm Hagit, Uriya Bekenstein, Bekenstein Uriya, Sagiv Shifman, Shifman Sagiv, Sebastian Kadener, Kadener Sebastian

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Frontiers in cellular neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

7 citing papers in PubMed, 12 citations in OpenAlex.

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4 · The record

Corrections and comments

  • Erratum issued
    Erratum: A new2013 · Varun, Pandey [corrected to Pandey, Varun]; Hagit, Turm [corrected to Turm, Hagit]; Uriya, Bekenstein [corrected to Bekenstein, Uriya]; Sagiv, Shifman [corrected to Shifman, Sagiv]; Sebastian, Kadener [corrected to Kadener, Sebastian]
5 · Who and what money

Authors and funding

10 authors at 1 institution in 1 country.

Varun PandeyBiological Chemistry Department, Silberman Institute of Life Sciences, The Hebrew University of Jerusalem Jerusalem, Israel.
Pandey VarunBiological Chemistry Department, Silberman Institute of Life Sciences, The Hebrew University of Jerusalem Jerusalem, Israel.
Hagit Turm
Turm Hagit
Uriya Bekenstein
Bekenstein Uriya
Sagiv Shifman
Shifman Sagiv
Sebastian Kadener
Kadener Sebastian
Hebrew University of Jerusalem · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pantothenate Kinase-Associated Neurodegeneration (PKAN) is a neurodegenerative disorder with a poorly understood molecular mechanism. It is caused by mutations in Pantothenate Kinase, the first enzyme in the Coenzyme A (CoA) biosynthetic pathway. Here, we developed a Drosophila model of PKAN (tim-fbl flies) that allows us to continuously monitor the modeled disease in the brain. In tim-fbl flies, downregulation of fumble, the Drosophila PanK homologue in the cells containing a circadian clock results in characteristic features of PKAN such as developmental lethality, hypersensitivity to oxidative stress, and diminished life span. Despite quasi-normal circadian transcriptional rhythms, tim-fbl flies display brain-specific aberrant circadian locomotor rhythms, and a unique transcriptional signature. Comparison with expression data from flies exposed to paraquat demonstrates that, as previously suggested, pathways others than oxidative stress are affected by PANK downregulation. Surprisingly we found a significant decrease in the expression of key components of the photoreceptor recycling pathways, which could lead to retinal degeneration, a hallmark of PKAN. Importantly, these defects are not accompanied by changes in structural components in eye genes suggesting that changes in gene expression in the eye precede and may cause the retinal degeneration. Indeed tim-fbl flies have diminished response to light transitions, and their altered day/night patterns of activity demonstrates defects in light perception. This suggest that retinal lesions are not solely due to oxidative stress and demonstrates a role for the transcriptional response to CoA deficiency underlying the defects observed in dPanK deficient flies. Moreover, in the present study we developed a new fly model that can be applied to other diseases and that allows the assessment of neurodegeneration in the brains of living flies.

Indexed as

circadianCoADrosophilaNBIAPanKPKAN

Identifiers

PMID24058333
PMCPMC3766815
OpenAlexW1511966979

What OpenQuestion holds

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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.