Evidence map›Paper›PMID 26190973›Full record

ArticleFrontiers in cellular neuroscience2015

Seeking homeostasis: temporal trends in respiration, oxidation, and calcium in SOD1 G93A Amyotrophic Lateral Sclerosis mice.

Cameron W Irvin, Renaid B Kim, Cassie S Mitchell

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

Article in Frontiers in cellular neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.

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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

3 authors at 1 institution in 1 country.

Cameron W IrvinDepartment of Biomedical Engineering, Georgia Institute of Technology - Emory University, Atlanta, GA USA.
Renaid B KimDepartment of Biomedical Engineering, Georgia Institute of Technology - Emory University, Atlanta, GA USA.
Cassie S MitchellDepartment of Biomedical Engineering, Georgia Institute of Technology - Emory University, Atlanta, GA USA.
Georgia Institute of Technology · US

Funding

Peripheral Reservoir of HIV DNA in Monocytes Pivotal to Cognition in HIVR01NS061696 · NINDS · UNIVERSITY OF HAWAII AT MANOA · PI VALCOUR, VICTOR · 2008 to 2012
$3.2M
A New Approach to ALSK01NS069616 · NINDS · GEORGIA INSTITUTE OF TECHNOLOGY · PI MITCHELL, CASSIE S · 2011 to 2015
$641k
Identification of Amyotrophic Lateral Sclerosis Clinical PredictorsR21NS081426 · NINDS · GEORGIA INSTITUTE OF TECHNOLOGY · PI MITCHELL, CASSIE S · 2013 to 2014
$389k
NINDS NIH HHS K01 NS069616NINDS NIH HHS R01 NS061696NINDS NIH HHS R21 NS081426
6 · The paper itself

Abstract

Impairments in mitochondria, oxidative regulation, and calcium homeostasis have been well documented in numerous Amyotrophic Lateral Sclerosis (ALS) experimental models, especially in the superoxide dismutase 1 glycine 93 to alanine (SOD1 G93A) transgenic mouse. However, the timing of these deficiencies has been debatable. In a systematic review of 45 articles, we examine experimental measurements of cellular respiration, mitochondrial mechanisms, oxidative markers, and calcium regulation. We evaluate the quantitative magnitude and statistical temporal trend of these aggregated assessments in high transgene copy SOD1 G93A mice compared to wild type mice. Analysis of overall trends reveals cellular respiration, intracellular adenosine triphosphate, and corresponding mitochondrial elements (Cox, cytochrome c, complex I, enzyme activity) are depressed for the entire lifespan of the SOD1 G93A mouse. Oxidant markers (H2O2, 8OH2'dG, MDA) are initially similar to wild type but are double that of wild type by the time of symptom onset despite early post-natal elevation of protective heat shock proteins. All aspects of calcium regulation show early disturbances, although a notable and likely compensatory convergence to near wild type levels appears to occur between 40 and 80 days (pre-onset), followed by a post-onset elevation in intracellular calcium. The identified temporal trends and compensatory fluctuations provide evidence that the "cause" of ALS may lay within failed homeostatic regulation, itself, rather than any one particular perturbing event or cellular mechanism. We discuss the vulnerabilities of motoneurons to regulatory instability and possible hypotheses regarding failed regulation and its potential treatment in ALS.

Indexed as

ALSCa2+energy metabolismmitochondriamotor neuron diseaseoxidative stress

Identifiers

PMID26190973
PMCPMC4486844
OpenAlexW1640935438

What OpenQuestion holds

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LicenceCC BY
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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.