Evidence map›Paper›PMID 34935299›Full record

ArticleBrain and behavior2022

The potential benefit of leptin therapy against amyotrophic lateral sclerosis (ALS).

Agueda Ferrer-Donato, Ana Contreras, Paloma Fernandez, Carmen M Fernandez-Martos

Open access · goldAbstract read
In one paragraph

Article in Brain and behavior, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.2field-weighted citation impact, top 18% 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

8 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Article
  3. Exploring the Role of Metabolic Hormones in Amyotrophic Lateral Sclerosis.International journal of molecular sciences · 2024
    Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. 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

4 authors at 3 institutions in 2 countries.

Agueda Ferrer-DonatoNeurometabolism Research Lab., Hospital Nacional de Paraplejicos, SESCAM, Toledo, Spain.
Ana ContrerasCentro de Investigación en Salud (CEINSA), Universidad de Almería, Almería, Spain.
Paloma FernandezInstitute of Applied Molecular Medicine (IMMA), Faculty of Medicine, Universidad San Pablo CEU, Madrid, Spain.
Carmen M Fernandez-MartosNeurometabolism Research Lab., Hospital Nacional de Paraplejicos, SESCAM, Toledo, Spain.ORCID 0000-0002-6387-4456
Ferrer Grupo (Spain) · ESUniversidad San Pablo CEU · ESUniversity of Tasmania · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTargeting leptin could represent a rational strategy to treat amyotrophic lateral sclerosis (ALS), as previously clinical studies have shown its levels to be associated with a lower risk of ALS disease. However, very little is known about the potential influence of leptin in altering disease progression in ALS, as it has thus far been correlated with the protection exerted by increased fat mass stores.

methodsWe studied the impact of leptin treatment beginning at 42-days of age (asymptomatic stage of disease) in the TDP-43 (TDP43

resultsOur study shows that leptin treatment was associated with altered expression of adipokines and metabolic proteins in TDP43

conclusionsCollectively, our results support leptin as a potential novel treatment approach for ALS.

Indexed as

Amyotrophic Lateral SclerosisAnimalsDisease Models, AnimalDisease ProgressionLeptinMiceMice, TransgenicLeptinamyotrophic lateral sclerosis (ALS)TAR DNA binding protein (TDP-43)

Identifiers

PMID34935299
PMCPMC8785645
OpenAlexW4200149406

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.