Evidence map›Paper›PMID 22485182›Full record

ArticlePloS one2012

Shared resistance to aging and ALS in neuromuscular junctions of specific muscles.

Gregorio Valdez, Juan C Tapia, Jeff W Lichtman, Michael A Fox, Joshua R Sanes

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 148 papers.

0numbers the graph read from it
0cells of the map it votes in
148citing papers in PubMed
10.5field-weighted citation impact, top 1% 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

148 citing papers in PubMed, 218 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. The Neuromuscular Junction: A Shared Vulnerability in Aging and Disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. MuSK Regulates Neuromuscular Junction Nav1.4 Localization and Excitability.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
    Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Building, Breaking, and Repairing Neuromuscular Synapses.Cold Spring Harbor perspectives in biology · 2024
    Review
  19. Review
  20. Article

88 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

5 authors at 2 institutions in 1 country.

Gregorio ValdezDepartment of Molecular and Cellular Biology and Center for Brain Science, Harvard University, Cambridge, Massachusetts, United States of America.
Juan C Tapia
Jeff W Lichtman
Michael A Fox
Joshua R Sanes
Harvard University · USVirginia Commonwealth University · US

Funding

Cellular and Molecular Analysis of Defects at Aging Neuromuscular SynapsesR01AG032322 · NIA · HARVARD UNIVERSITY · PI LICHTMAN, JEFF W, SANES, JOSHUA R · 2008 to 2012
$1.7M
NIA NIH HHS R01 AG032322NIA NIH HHS R01AG032322
6 · The paper itself

Abstract

Normal aging and neurodegenerative diseases both lead to structural and functional alterations in synapses. Comparison of synapses that are generally similar but respond differently to insults could provide the basis for discovering mechanisms that underlie susceptibility or resistance to damage. Here, we analyzed skeletal neuromuscular junctions (NMJs) in 16 mouse muscles to seek such differences. We find that muscles respond in one of three ways to aging. In some, including most limb and trunk muscles, age-related alterations to NMJs are progressive and extensive during the second postnatal year. NMJs in other muscles, such as extraocular muscles, are strikingly resistant to change. A third set of muscles, including several muscles of facial expression and the external anal sphinter, succumb to aging but not until the third postnatal year. We asked whether susceptible and resistant muscles differed in rostrocaudal or proximodistal position, source of innervation, motor unit size, or fiber type composition. Of these factors, muscle innervation by brainstem motor neurons correlated best with resistance to age-related decline. Finally, we compared synaptic alterations in normally aging muscles to those in a mouse model of amyotrophic lateral sclerosis (ALS). Patterns of resistance and susceptibility were strikingly correlated in the two conditions. Moreover, damage to NMJs in aged muscles correlated with altered expression and distribution of CRMP4a and TDP-43, which are both altered in motor neurons affected by ALS. Together, these results reveal novel structural, regional and molecular parallels between aging and ALS.

Indexed as

AgingAmyotrophic Lateral SclerosisAnimalsDNA-Binding ProteinsGene ExpressionGene Expression RegulationMiceMice, Inbred C57BLMice, TransgenicMotor NeuronsMuscle Fibers, SkeletalMuscle, SkeletalMutation, MissenseNerve Tissue ProteinsNeuromuscular JunctionReceptors, CholinergicDNA-Binding ProteinsDpysl3 protein, mouseNerve Tissue ProteinsReceptors, CholinergicSod1 protein, mouseSuperoxide DismutaseSuperoxide Dismutase-1

Identifiers

PMID22485182
PMCPMC3317643
OpenAlexW2156326705

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.