Evidence map›Paper›PMID 24524276›Full record

ArticleBMC neuroscience2014

Mitochondrial oxygen consumption deficits in skeletal muscle isolated from an Alzheimer's disease-relevant murine model.

Rosemary A Schuh, Kathryn C Jackson, Anna E Schlappal, Espen E Spangenburg, Christopher W Ward, Ji H Park, Natalie Dugger, Guo Li Shi, Paul S Fishman

Open access · goldAbstract read
In one paragraph

Article in BMC neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

24 citing papers in PubMed, 36 citations in OpenAlex.

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  17. An Exploratory Analysis of Potential New Biomarkers of Cognitive Function.The journals of gerontology. Series A, Biological sciences and medical sciences · 2019
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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

9 authors at 3 institutions in 1 country.

Rosemary A SchuhResearch Service, VAMHCS, 10 North Greene Street, 3C-125, Baltimore, Maryland 21201, USA. rschu003@umaryland.edu.
Kathryn C Jackson
Anna E Schlappal
Espen E Spangenburg
Christopher W Ward
Ji H Park
Natalie Dugger
Guo Li Shi
Paul S Fishman
VA Maryland Health Care System · USUniversity of Maryland, College Park · USUniversity of Maryland, Baltimore · US

Funding

The role of BRCA1 in regulation of lipid metabolism in skeletal muscleR21AR059913 · NIAMS · UNIV OF MARYLAND, COLLEGE PARK · PI SPANGENBURG, ESPEN E · 2011 to 2012
$361k
Estrogen-Derived Para-Quinol Intervention in Alzheimer's DiseaseR21AG031387 · NIA · UNIV OF MARYLAND, COLLEGE PARK · PI OTTINGER, MARY ANN · 2009 to 2010
$355k
NIAMS NIH HHS AR059913-EESNIA NIH HHS AG000268-KCJNIA NIH HHS AG031387-MA
6 · The paper itself

Abstract

backgroundAge is considered a primary risk factor for neurodegenerative diseases including Alzheimer's disease (AD). It is also now well understood that mitochondrial function declines with age. Mitochondrial deficits have been previously assessed in brain from both human autopsy tissue and disease-relevant transgenic mice. Recently it has been recognized that abnormalities of muscle may be an intrinsic aspect of AD and might contribute to the pathophysiology. However, deficits in mitochondrial function have yet to be clearly assessed in tissues outside the central nervous system (CNS). In the present study, we utilized a well-characterized AD-relevant transgenic mouse strain to assess mitochondrial respiratory deficits in both brain and muscle. In addition to mitochondrial function, we assessed levels of transgene-derived amyloid precursor protein (APP) in homogenates isolated from brain and muscle of these AD-relevant animals.

resultsWe now demonstrate that skeletal muscles isolated from these animals have differential levels of mutant full-length APP depending on muscle type. Additionally, isolated muscle fibers from young transgenic mice (3 months) have significantly decreased maximal mitochondrial oxygen consumption capacity compared to non-transgenic, age-matched mice, with similar deficits to those previously described in brain.

conclusionsThis is the first study to directly examine mitochondrial function in skeletal muscle from an AD-relevant transgenic murine model. As with brain, these deficits in muscle are an early event, occurring prior to appearance of amyloid plaques.

Indexed as

Disease Models, AnimalOxygen ConsumptionAgingAlzheimer DiseaseAnimalsCells, CulturedHumansMiceMice, Inbred C57BLMice, TransgenicMitochondria, MuscleMuscle, SkeletalOxygenOxygen

Identifiers

PMID24524276
PMCPMC3930757
OpenAlexW2034245339

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.