Evidence map›Paper›PMID 29449528›Full record

ArticleCell death & disease2018

ALS-related human cortical and motor neurons survival is differentially affected by Sema3A.

Anastasya Birger, Miri Ottolenghi, Liat Perez, Benjamin Reubinoff, Oded Behar

Abstract readComparative Study
In one paragraph

Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
–field-weighted citation impact
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

15 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. Article
  10. Semaphorins in Adult Nervous System Plasticity and Disease.Frontiers in synaptic neuroscience · 2021
    Review
  11. Article
  12. Review
  13. Article
  14. Motor Neuron Susceptibility in ALS/FTD.Frontiers in neuroscience · 2019
    Review
  15. miR126-5p Downregulation Facilitates Axon Degeneration and NMJ Disruption via a Non-Cell-Autonomous Mechanism in ALS.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018
    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

5 authors.

Anastasya BirgerDepartment of Developmental Biology and Cancer Research, Institute of Medical Research Israel-Canada (IMRIC), Faculty of Medicine, The Hebrew University, P.O. Box 12272, 91120, Jerusalem, Israel.
Miri OttolenghiThe Sidney and Judy Swartz Embryonic Stem Cell Research Center of The Goldyne Savad Institute of Gene Therapy & The Department of Obstetrics, Hadassah University Medical Center, Jerusalem, 91120, Israel.
Liat PerezDepartment of Developmental Biology and Cancer Research, Institute of Medical Research Israel-Canada (IMRIC), Faculty of Medicine, The Hebrew University, P.O. Box 12272, 91120, Jerusalem, Israel.
Benjamin ReubinoffThe Sidney and Judy Swartz Embryonic Stem Cell Research Center of The Goldyne Savad Institute of Gene Therapy & The Department of Obstetrics, Hadassah University Medical Center, Jerusalem, 91120, Israel. BenR@hadassah.org.il.
Oded BeharDepartment of Developmental Biology and Cancer Research, Institute of Medical Research Israel-Canada (IMRIC), Faculty of Medicine, The Hebrew University, P.O. Box 12272, 91120, Jerusalem, Israel. odedb@ekmd.huji.ac.il.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by cell death of upper and lower motor neurons (MNs). The cause of MN cell loss is not completely understood but involves both cell autonomous and non-cell autonomous mechanisms. Numerous molecules have been implicated to be involved in the death of MNs. One such candidate is semaphorin 3A (Sema3A). In ALS patients, Sema3A was shown to be significantly upregulated in the motor cortex and downregulated in the spinal cord. In the mouse, Sema3A was shown to be an axon repellent molecule for MNs. Sema3A could also induce death of different neuronal types that are also repelled by it, including sensory, sympathetic, retinal, and cortical neurons. In contrast, astrocyte-specific knockout of Sema3A results in motor neuron cell death, consistent with the idea that Sema3A is a survival factor for mouse motor neurons. Here, we tested the response of human cortical neurons and spinal cord MNs to Sema3A. We found that Sema3A enhances the survival of spinal cord MNs. In contrast, Sema3A reduces the survival of cortical neurons. Thus, both upregulation of Sema3A in the cortex, or downregulation in the spinal cord of ALS patients is likely to directly contribute to MNs cell loss in ALS patients.

Indexed as

Amyotrophic Lateral SclerosisCell DeathCell LineCell SurvivalCerebral CortexHumansMotor NeuronsNeuropilinsSemaphorin-3ASpinal NervesNeuropilinsSEMA3A protein, humanSemaphorin-3A

Identifiers

PMID29449528
PMCPMC5833799

What Socratic 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 Socratic graph.