Evidence map›Paper›PMID 28874134›Full record

ArticleBMC neurology2017

Amyotrophic lateral sclerosis modifies progenitor neural proliferation in adult classic neurogenic brain niches.

Lucía Galán, Ulises Gómez-Pinedo, Antonio Guerrero, Jose Manuel García-Verdugo, Jorge Matías-Guiu

Open access · goldAbstract read
In one paragraph

Article in BMC neurology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
3.0field-weighted citation impact, top 9% 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

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 77 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. BML-281 promotes neuronal differentiation by modulating Wnt/CaMolecular and cellular biochemistry · 2024
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  13. Review
  14. Neurogenesis and Viral Infection.Frontiers in immunology · 2022
    Review
  15. Article
  16. Article
  17. Reconditioning the Neurogenic Niche of Adult Non-human Primates by Antisense Oligonucleotide-Mediated Attenuation of TGFβ Signaling.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021
    Article
  18. Article
  19. Review
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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

5 authors at 2 institutions in 1 country.

Lucía GalánAmyotrophic Lateral Sclerosis Unit, Department of Neurology, Hospital Clínico San Carlos, Calle Profesor Martín Lagos s/n, 28040, Madrid, Spain. elainvestigacion@luciagalan.es.
Ulises Gómez-PinedoInstitute of Neurosciences, Hospital Clínico San Carlos, Madrid, Spain.
Antonio GuerreroAmyotrophic Lateral Sclerosis Unit, Department of Neurology, Hospital Clínico San Carlos, Calle Profesor Martín Lagos s/n, 28040, Madrid, Spain.
Jose Manuel García-VerdugoCavanilles Institute of Biodiversity and Evolutionary Biology, Comparative Neurobiology Unit, Universidad de Valencia, Paterna, Spain.
Jorge Matías-GuiuInstitute of Neurosciences, Hospital Clínico San Carlos, Madrid, Spain.
Hospital Clínico San Carlos · ESParc Científic de la Universitat de València · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAdult neurogenesis persists through life at least in classic neurogenic niches. Neurogenesis has been previously described as reduced in neurodegenerative diseases. There is not much knowledge about is adult neurogenesis is or not modified in amyotrophy lateral sclerosis (ALS). All previous publications has studied the ALS SOD1 (superoxide dismutase) transgenic mouse model. The purpose of this study is to examine the process of adult neurogenesis in classic niches (subventricular zone [SVZ] and subgranular zone [SGZ] of the dentate gyrus) in patients with amyotrophic lateral sclerosis (ALS), both with (ALS-FTD) and without associated frontotemporal dementia (FTD).

methodsWe studied 9 autopsies of patients with ALS (including 2 with ALS-FTD) and 4 controls. ALS was confirmed histologically. Studies of the SVZ and SGZ were conducted using markers of proliferation (Ki-67, PCNA), of pluripotent neural progenitor cells (GFAPδ), neuroblasts (PSA-NCAM, DCX, TUJ1), and an astrocyte marker (GFAP). Results were analyzed with non-parametric tests. We then studied correlations between the different markers and the percentage of phosphorylated TDP-43 (pTDP-43).

resultsWe observed a statistically significant increase in proliferation in the SVZ in all patients with ALS. While this increase was more marked in ALS forms associated with dementia, the small sample size does not permit a statistical subgroup analysis. In contrast, proliferation in the SGZ was decreased in all patients. These alterations showed a positive and direct correlation with the percentage of pTDP-43 in the SVZ, and a negative, exponential correlation with that percentage in the SGZ.

conclusionsWe observed alterations of the proliferation of neural progenitor in classic adult neurogenic niches in patients with ALS. The 2 neurogenic niches exhibited opposite changes such that proliferation increased in the SVZ and decreased in the SGZ.

Indexed as

AgedAged, 80 and overAmyotrophic Lateral SclerosisBrainDoublecortin ProteinFemaleFrontotemporal DementiaHumansLateral VentriclesMaleMiddle AgedNeural Stem CellsNeurogenesisDoublecortin ProteinAdult neurogenesisAmyotrophic lateral sclerosisFrontotemporal dementiaNeurodegenerative diseasesTDP-43

Identifiers

PMID28874134
PMCPMC5585932
OpenAlexW2752373406

What OpenQuestion holds

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Registered trials

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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.