Evidence map›Paper›PMID 35287738›Full record

ArticleTranslational neurodegeneration2022

Impaired glymphatic function in the early stages of disease in a TDP-43 mouse model of amyotrophic lateral sclerosis.

Akram Zamani, Adam K Walker, Ben Rollo, Katie L Ayers, Raysha Farah, Terence J O'Brien, David K Wright

Open access · goldAbstract read
In one paragraph

Article in Translational neurodegeneration, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 2 pooled it
6.7field-weighted citation impact, top 2% 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

35 citing papers in PubMed, 2 syntheses or guidelines pooled it, 63 citations in OpenAlex.

  1. Pooled it
  2. Glymphatic System a Window on TBI Pathophysiology: A Systematic Review.International journal of molecular sciences · 2022
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  20. Global brain activity and its coupling with cerebrospinal fluid flow is related to tau pathology.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024
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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

7 authors at 4 institutions in 1 country.

Akram ZamaniDepartment of Neuroscience, Central Clinical School, Monash University, Melbourne, VIC, 3004, Australia.
Adam K WalkerQueensland Brain Institute, The University of Queensland, St Lucia, QLD, 4072, Australia.
Ben RolloDepartment of Neuroscience, Central Clinical School, Monash University, Melbourne, VIC, 3004, Australia.
Katie L AyersThe Murdoch Children's Research Institute, The Royal Children's Hospital, Parkville, VIC, 3052, Australia.
Raysha FarahDepartment of Neuroscience, Central Clinical School, Monash University, Melbourne, VIC, 3004, Australia.
Terence J O'BrienDepartment of Neuroscience, Central Clinical School, Monash University, Melbourne, VIC, 3004, Australia.
David K WrightDepartment of Neuroscience, Central Clinical School, Monash University, Melbourne, VIC, 3004, Australia. david.wright@monash.edu.ORCID 0000-0002-7535-8651
Monash University · AURoyal Children's Hospital · AUThe Royal Melbourne Hospital · AUThe University of Queensland · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMultiple lines of evidence suggest possible impairment of the glymphatic system in amyotrophic lateral sclerosis (ALS). To investigate this, we used in vivo magnetic resonance imaging (MRI) to assess glymphatic function early in the course of disease in a transgenic mouse with doxycycline (Dox)-controlled expression of cytoplasmic human TDP-43 (hTDP-43ΔNLS), mimicking the key pathology implicated in ALS.

methodsAdult TDP-43 transgenic and littermate monogenic control mice underwent longitudinal multimodal MRI one and three weeks after the cessation of Dox feed, together with weekly rotarod assessments of motor performance. Glymphatic function was assessed using dynamic contrast-enhanced MRI to track the clearance of an MR contrast agent injected into the cisterna magna.

resultsCompared to their littermate controls, TDP-43 mice exhibited progressive neurodegeneration including that within the primary motor cortex, primary somatosensory cortex and corticospinal tract, significant weight loss including gastrocnemius atrophy, and shortened telomere length. Furthermore, in the presence of this ALS-like phenotype, these mice have significantly disrupted glymphatic function.

conclusionsAlthough the relationship between glymphatic clearance and ALS disease progression remains to be elucidated, these changes occurred very early in the disease course. This provides initial evidence to suggest that the glymphatic system might be a potential therapeutic target in the treatment of ALS.

Indexed as

Amyotrophic Lateral SclerosisAnimalsDisease Models, AnimalDisease ProgressionDNA-Binding ProteinsMiceMice, TransgenicTelomereTelomere ShorteningDNA-Binding ProteinsTardbp protein, mouseCerebrospinal fluidDiffusion-weighted imagingMagnetic resonance imagingNeurodegenerationTelomere

Identifiers

PMID35287738
PMCPMC8922788
OpenAlexW4221056323

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.