Evidence map›Paper›PMID 36704819›Full record

ReviewJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism2023

Blood-CNS barrier dysfunction in amyotrophic lateral sclerosis: Proposed mechanisms and clinical implications.

Moritz Steinruecke, Rebecca Murphy Lonergan, Bhuvaneish T Selvaraj, Siddharthan Chandran, Blanca Diaz-Castro, Maria Stavrou

Open access · hybridAbstract readReview
In one paragraph

Review in Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
10.9field-weighted citation impact, top 1% 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

37 citing papers in PubMed, 53 citations in OpenAlex.

  1. Article
  2. Review
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  6. Article
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  8. Exosome Proteomics of SOD1Annals of clinical and translational neurology · 2026
    Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Astrocytes as Therapeutic Targets in Neurodegenerative Disorders.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
    Review
  14. Article
  15. Article
  16. 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

6 authors at 3 institutions in 1 country.

Moritz SteinrueckeEdinburgh Medical School, The University of Edinburgh, Edinburgh, UK.ORCID 0000-0003-1647-4481
Rebecca Murphy LonerganNorth Middlesex University Hospital NHS Trust, London, UK.
Bhuvaneish T SelvarajEuan MacDonald Centre for MND Research, The University of Edinburgh, Edinburgh, UK.
Siddharthan ChandranEuan MacDonald Centre for MND Research, The University of Edinburgh, Edinburgh, UK.
Blanca Diaz-CastroCentre for Clinical Brain Sciences, The University of Edinburgh, Edinburgh, UK.
Maria StavrouEuan MacDonald Centre for MND Research, The University of Edinburgh, Edinburgh, UK.
UK Dementia Research Institute · GBNorth Middlesex University Hospital NHS Trust · GBUniversity of Cambridge · GB

Funding

Medical Research Council MC_EX_MR/N50192X/1Medical Research Council MR/T000708/1
6 · The paper itself

Abstract

There is strong evidence for blood-brain and blood-spinal cord barrier dysfunction at the early stages of many neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS). Since impairment of the blood-central nervous system barrier (BCNSB) occurs during the pre-symptomatic stages of ALS, the mechanisms underlying this pathology are likely also involved in the ALS disease process. In this review, we explore how drivers of ALS disease, particularly mitochondrial dysfunction, astrocyte pathology and neuroinflammation, may contribute to BCNSB impairment. Mitochondria are highly abundant in BCNSB tissue and mitochondrial dysfunction in ALS contributes to motor neuron death. Likewise, astrocytes adopt key physical, transport and metabolic functions at the barrier, many of which are impaired in ALS. Astrocytes also show raised expression of inflammatory markers in ALS and ablating ALS-causing transgenes in astrocytes slows disease progression. In addition, key drivers of neuroinflammation, including TAR DNA-binding protein 43 (TDP-43) pathology, matrix metalloproteinase activation and systemic inflammation, affect BCNSB integrity in ALS. Finally, we discuss the translational implications of BCNSB dysfunction in ALS, including the development of biomarkers for disease onset and progression, approaches aimed at restoring BCNSB integrity and

Indexed as

Amyotrophic Lateral SclerosisAnimalsAstrocytesDisease Models, AnimalHumansMotor NeuronsNeuroinflammatory DiseasesSpinal CordAmyotrophic lateral sclerosisastrocytesblood-CNS barriermitochondrianeuroinflammation

Identifiers

PMID36704819
PMCPMC10108188
OpenAlexW4318205373

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.