Evidence map›Paper›PMID 38965379›Full record

ReviewNature reviews. Neurology2024

Brain-body mechanisms contribute to sexual dimorphism in amyotrophic lateral sclerosis.

Sarah M Jacob, Sukyoung Lee, Seung Hyun Kim, Keith A Sharkey, Gerald Pfeffer, Minh Dang Nguyen

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Neurology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
–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

14 citing papers in PubMed, 1 synthesis or guideline pooled it.

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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

6 authors.

Sarah M JacobHotchkiss Brain Institute, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada.
Sukyoung LeeHotchkiss Brain Institute, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada.
Seung Hyun KimDepartment of Neurology, Hanyang University Hospital, Seoul, South Korea.
Keith A SharkeyHotchkiss Brain Institute, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada.ORCID 0000-0001-9560-1711
Gerald PfefferHotchkiss Brain Institute, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada. gerald.pfeffer@ucalgary.ca.
Minh Dang NguyenHotchkiss Brain Institute, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada. mdnguyen@ucalgary.ca.ORCID 0000-0003-4547-8617

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Amyotrophic lateral sclerosis (ALS) is the most common form of human motor neuron disease. It is characterized by the progressive degeneration of upper and lower motor neurons, leading to generalized motor weakness and, ultimately, respiratory paralysis and death within 3-5 years. The disease is shaped by genetics, age, sex and environmental stressors, but no cure or routine biomarkers exist for the disease. Male individuals have a higher propensity to develop ALS, and a different manifestation of the disease phenotype, than female individuals. However, the mechanisms underlying these sex differences remain a mystery. In this Review, we summarize the epidemiology of ALS, examine the sexually dimorphic presentation of the disease and highlight the genetic variants and molecular pathways that might contribute to sex differences in humans and animal models of ALS. We advance the idea that sexual dimorphism in ALS arises from the interactions between the CNS and peripheral organs, involving vascular, metabolic, endocrine, musculoskeletal and immune systems, which are strikingly different between male and female individuals. Finally, we review the response to treatments in ALS and discuss the potential to implement future personalized therapeutic strategies for the disease.

Indexed as

Amyotrophic Lateral SclerosisSex CharacteristicsAnimalsBrainFemaleHumansMale

Identifiers

What OpenQuestion holds

Textmetadata
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.