Evidence map›Paper›PMID 32380032›Full record

ArticleNeuron2020

Presynaptic Homeostasis Opposes Disease Progression in Mouse Models of ALS-Like Degeneration: Evidence for Homeostatic Neuroprotection.

Brian O Orr, Anna G Hauswirth, Barbara Celona, Richard D Fetter, Giulia Zunino, Evgeny Z Kvon, Yiwen Zhu, Len A Pennacchio, Brian L Black, Graeme W Davis

Open access · bronzeAbstract read
In one paragraph

Article in Neuron, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
4.1field-weighted citation impact, top 4% 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

36 citing papers in PubMed, 59 citations in OpenAlex.

  1. Temporal and Cell-Specific Regulation of Synaptic Homeostasis by the Chromatin Remodeler Chd1.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  2. Transsynaptic linking of calcium channels and postsynaptic receptors at a dyadic synapse.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  3. Robust PHP in Adult Hippocampus: Essential Assay Optimizations.bioRxiv : the preprint server for biology · 2026
    Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Behavioral resilience via dynamic circuit firing homeostasis.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  10. CaCell reports · 2025
    Article
  11. Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Post-synaptic GABACell reports · 2023
    Article
  17. Article
  18. Glial Sphingosine-Mediated Epigenetic Regulation Stabilizes Synaptic Function inThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
  19. Synaptic Dysfunction and Plasticity in Amyotrophic Lateral Sclerosis.International journal of molecular sciences · 2023
    Review
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 3 institutions in 1 country.

Brian O OrrDepartment of Biochemistry and Biophysics, Kavli Institute for Fundamental Neuroscience, University of California, San Francisco, CA 94941, USA.
Anna G HauswirthDepartment of Biochemistry and Biophysics, Kavli Institute for Fundamental Neuroscience, University of California, San Francisco, CA 94941, USA.
Barbara CelonaCardiovascular Research Institute, University of California, San Francisco, CA, USA.
Richard D FetterDepartment of Biochemistry and Biophysics, Kavli Institute for Fundamental Neuroscience, University of California, San Francisco, CA 94941, USA.
Giulia ZuninoDepartment of Biochemistry and Biophysics, Kavli Institute for Fundamental Neuroscience, University of California, San Francisco, CA 94941, USA.
Evgeny Z KvonEnvironmental Genomics and Systems Biology Division, Lawrence Berkeley National Laboratory, Berkeley, CA 94720, USA.
Yiwen ZhuEnvironmental Genomics and Systems Biology Division, Lawrence Berkeley National Laboratory, Berkeley, CA 94720, USA.
Len A PennacchioEnvironmental Genomics and Systems Biology Division, Lawrence Berkeley National Laboratory, Berkeley, CA 94720, USA; U.S. Department of Energy Joint Genome Institute, Walnut Creek, CA 94598, USA; Comparative Biochemistry Program, University of California, Berkeley, CA 94720, USA.
Brian L BlackCardiovascular Research Institute, University of California, San Francisco, CA, USA.
Graeme W DavisDepartment of Biochemistry and Biophysics, Kavli Institute for Fundamental Neuroscience, University of California, San Francisco, CA 94941, USA. Electronic address: graeme.davis@UCSF.edu.
University of California, San Francisco · USLawrence Berkeley National Laboratory · USJoint Genome Institute · US

Funding

MEDICAL SCIENTIST TRAINING PROGRAMT32GM007618 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI ANDERSON, MARK S · 1985 to 2020
$29.6M
Generation of an In Vivo Human Genome Transcriptional Enhancer DatasetR01HG003988 · NHGRI · UNIVERSITY OF CALIF-LAWRENC BERKELEY LAB · PI Len Alexander Pennacchio · 2006 to 2026
$24.1M
Project 3: Control of cardiac transcription by MEF2 and myocardinP01HL146366 · NHLBI · J. DAVID GLADSTONE INSTITUTES · PI KROGAN, NEVAN J · 2019 to 2023
$13.7M
Homeostatic Stabilization of Neural Function in Health and DiseaseR35NS097212 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI DAVIS, GRAEME W · 2017 to 2024
$9.2M
Functional assessment of enhancer-gene interactions in vivoK99HG009682 · NHGRI · UNIVERSITY OF CALIF-LAWRENC BERKELEY LAB · PI KVON, EVGENY · 2017 to 2018
$263k
NHGRI NIH HHS K99 HG009682NHGRI NIH HHS R01 HG003988NHLBI NIH HHS P01 HL146366NIGMS NIH HHS T32 GM007618NINDS NIH HHS R35 NS097212
6 · The paper itself

Abstract

Progressive synapse loss is an inevitable and insidious part of age-related neurodegenerative disease. Typically, synapse loss precedes symptoms of cognitive and motor decline. This suggests the existence of compensatory mechanisms that can temporarily counteract the effects of ongoing neurodegeneration. Here, we demonstrate that presynaptic homeostatic plasticity (PHP) is induced at degenerating neuromuscular junctions, mediated by an evolutionarily conserved activity of presynaptic ENaC channels in both Drosophila and mouse. To assess the consequence of eliminating PHP in a mouse model of ALS-like degeneration, we generated a motoneuron-specific deletion of Scnn1a, encoding the ENaC channel alpha subunit. We show that Scnn1a is essential for PHP without adversely affecting baseline neural function or lifespan. However, Scnn1a knockout in a degeneration-causing mutant background accelerated motoneuron loss and disease progression to twice the rate observed in littermate controls with intact PHP. We propose a model of neuroprotective homeostatic plasticity, extending organismal lifespan and health span.

Indexed as

Amyotrophic Lateral SclerosisAnimalsDisease Models, AnimalDisease ProgressionDrosophila melanogasterEpithelial Sodium ChannelsHomeostasisMiceMice, KnockoutNeuromuscular JunctionNeuronal PlasticityNeuroprotectionPresynaptic TerminalsEpithelial Sodium ChannelsScnn1a protein, mouseAmyotrophic Lateral SclerosisastrocytebenzamilENaChomeostatic plasticityneurodegenerationneuroprotectionNMJpresynaptic releasespinal cord

Identifiers

PMID32380032
PMCPMC7529479
OpenAlexW3021296578

What OpenQuestion holds

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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.