Evidence map›Paper›PMID 34082828›Full record

ArticleActa neuropathologica communications2021

Pathology of the neurovascular unit in leukodystrophies.

Parand Zarekiani, Marjolein Breur, Nicole I Wolf, Helga E de Vries, Marjo S van der Knaap, Marianna Bugiani

Open access · goldAbstract read
In one paragraph

Article in Acta neuropathologica communications, 2021. 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
0.7field-weighted citation impact, top 31% 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, 14 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Nucleotide metabolism, leukodystrophies, and CNS pathology.Journal of inherited metabolic disease · 2024
    Review
  5. Article
  6. Article
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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 2 institutions in 1 country.

Parand ZarekianiDepartment of Pathology, Amsterdam UMC, Vrije Universiteit Amsterdam and Amsterdam Neuroscience, de Boelelaan 1117, 1081HV, Amsterdam, The Netherlands.ORCID 0000-0001-7760-7247
Marjolein BreurAmsterdam Leukodystrophy Center, Amsterdam UMC, Amsterdam, The Netherlands.
Nicole I WolfAmsterdam Leukodystrophy Center, Amsterdam UMC, Amsterdam, The Netherlands.
Helga E de VriesDepartment of Molecular Cell Biology and Immunology, Amsterdam UMC, Vrije Universiteit Amsterdam and Amsterdam Neuroscience, Amsterdam, The Netherlands.
Marjo S van der KnaapAmsterdam Leukodystrophy Center, Amsterdam UMC, Amsterdam, The Netherlands.
Marianna BugianiDepartment of Pathology, Amsterdam UMC, Vrije Universiteit Amsterdam and Amsterdam Neuroscience, de Boelelaan 1117, 1081HV, Amsterdam, The Netherlands. m.bugiani@amsterdamumc.nl.
Amsterdam Neuroscience · NLEmma Kinderziekenhuis · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The blood-brain barrier is a dynamic endothelial cell barrier in the brain microvasculature that separates the blood from the brain parenchyma. Specialized brain endothelial cells, astrocytes, neurons, microglia and pericytes together compose the neurovascular unit and interact to maintain blood-brain barrier function. A disturbed brain barrier function is reported in most common neurological disorders and may play a role in disease pathogenesis. However, a comprehensive overview of how the neurovascular unit is affected in a wide range of rare disorders is lacking. Our aim was to provide further insights into the neuropathology of the neurovascular unit in leukodystrophies to unravel its potential pathogenic role in these diseases. Leukodystrophies are monogenic disorders of the white matter due to defects in any of its structural components. Single leukodystrophies are exceedingly rare, and availability of human tissue is unique. Expression of selective neurovascular unit markers such as claudin-5, zona occludens 1, laminin, PDGFRβ, aquaporin-4 and α-dystroglycan was investigated in eight different leukodystrophies using immunohistochemistry. We observed tight junction rearrangements, indicative of endothelial dysfunction, in five out of eight assessed leukodystrophies of different origin and an altered aquaporin-4 distribution in all. Aquaporin-4 redistribution indicates a general astrocytic dysfunction in leukodystrophies, even in those not directly related to astrocytic pathology or without prominent reactive astrogliosis. These findings provide further evidence for dysfunction in the orchestration of the neurovascular unit in leukodystrophies and contribute to a better understanding of the underlying disease mechanism.

Indexed as

AdolescentAdultAgedAlexander DiseaseAutoimmune Diseases of the Nervous SystemBlood-Brain BarrierChildChild, PreschoolFemaleHumansLeukodystrophy, MetachromaticMaleNervous System MalformationsNeurovascular CouplingPelizaeus-Merzbacher DiseaseAstrocytesEndotheliumLeukodystrophyMicrogliaMyelinNeurovascular unitOligodendrocytePericyteWhite matter

Identifiers

PMID34082828
PMCPMC8173888
OpenAlexW3164599534

What OpenQuestion holds

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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.