Evidence map›Paper›PMID 26322226›Full record

ArticleCell regeneration (London, England)2015

The interplay between metabolic homeostasis and neurodegeneration: insights into the neurometabolic nature of amyotrophic lateral sclerosis.

S T Ngo, F J Steyn

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell regeneration (London, England), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
4.0field-weighted citation impact, top 7% 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

32 citing papers in PubMed, 46 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Exploring the Role of Metabolic Hormones in Amyotrophic Lateral Sclerosis.International journal of molecular sciences · 2024
    Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. In-depth triacylglycerol profiling using MSAnalytica chimica acta · 2021
    Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. 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

2 authors at 2 institutions in 1 country.

S T NgoQueensland Brain Institute, The University of Queensland, St Lucia, Brisbane 4072 Australia ; School of Biomedical Sciences, The University of Queensland, St Lucia, Brisbane 4072 Australia ; Department of Neurology, Royal Brisbane and Women's Hospital, Herston, Brisbane 4006 Australia ; University of Queensland Centre for Clinical Research, The University of Queensland, Herston, Brisbane, 4029 Australia.
F J SteynSchool of Biomedical Sciences, The University of Queensland, St Lucia, Brisbane 4072 Australia ; University of Queensland Centre for Clinical Research, The University of Queensland, Herston, Brisbane, 4029 Australia.
Royal Brisbane and Women's Hospital · AUUniversity of Queensland · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Amyotrophic lateral sclerosis (ALS) is a fatal, neurodegenerative disease that is characterized by the selective degeneration of upper motor neurons and lower spinal motor neurons, resulting in the progressive paralysis of all voluntary muscles. Approximately 10 % of ALS cases are linked to known genetic mutations, with the remaining 90 % of cases being sporadic. While the primary pathology in ALS is the selective death of upper and lower motor neurons, numerous studies indicate that an imbalance in whole body and/or cellular metabolism influences the rate of progression of disease. This review summarizes current research surrounding the impact of impaired metabolic physiology in ALS. We extend ideas to consider prospects that lie ahead in terms of how metabolic alterations may impact the selective degeneration of neurons in ALS and how targeting of adenosine triphosphate-sensitive potassium (KATP) channels may represent a promising approach for obtaining neuroprotection in ALS.

Indexed as

Amyotrophic lateral sclerosisHyperexcitabilityIon channelsKATP channelsMetabolismNeurometabolism

Identifiers

PMID26322226
PMCPMC4551561
OpenAlexW1834999442

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.