Evidence map›Paper›PMID 38627751›Full record

ArticleJournal of biomedical science2024

Longitudinal alterations in brain perfusion and vascular reactivity in the zQ175DN mouse model of Huntington's disease.

Tamara Vasilkovska, Somaie Salajeghe, Verdi Vanreusel, Johan Van Audekerke, Marlies Verschuuren, Lydiane Hirschler, Jan Warnking, Isabel Pintelon, Dorian Pustina, Roger Cachope and 6 more

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of biomedical science, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

6 citing papers in PubMed, 7 citations in OpenAlex.

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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

16 authors at 4 institutions in 5 countries.

Tamara VasilkovskaBio-Imaging Lab, University of Antwerp, Universiteitsplein 1, 2610 Wilrijk, Antwerp, Belgium. tamara.vasilkovska@uantwerpen.be.ORCID http://orcid.org/0000-0001-7611-3966
Somaie SalajegheBio-Imaging Lab, University of Antwerp, Universiteitsplein 1, 2610 Wilrijk, Antwerp, Belgium.
Verdi VanreuselBio-Imaging Lab, University of Antwerp, Universiteitsplein 1, 2610 Wilrijk, Antwerp, Belgium.
Johan Van AudekerkeBio-Imaging Lab, University of Antwerp, Universiteitsplein 1, 2610 Wilrijk, Antwerp, Belgium.
Marlies VerschuurenµNEURO Research Centre of Excellence, University of Antwerp, Antwerp, Belgium.
Lydiane HirschlerC.J. Gorter MRI Center, Leiden University Medical Center, Leiden, the Netherlands.
Jan WarnkingUniv. Grenoble Alpes, Inserm, U1216, Grenoble Institut Neurosciences, Grenoble, France.
Isabel PintelonµNEURO Research Centre of Excellence, University of Antwerp, Antwerp, Belgium.
Dorian PustinaCHDI Management, Inc., the company that manages the scientific activities of CHDI Foundation, Inc, Princeton, NJ, USA.
Roger CachopeCHDI Management, Inc., the company that manages the scientific activities of CHDI Foundation, Inc, Princeton, NJ, USA.
Ladislav MrzljakCHDI Management, Inc., the company that manages the scientific activities of CHDI Foundation, Inc, Princeton, NJ, USA.
Ignacio Muñoz-SanjuanCHDI Management, Inc., the company that manages the scientific activities of CHDI Foundation, Inc, Princeton, NJ, USA.
Emmanuel L BarbierUniv. Grenoble Alpes, Inserm, U1216, Grenoble Institut Neurosciences, Grenoble, France.
Winnok H De VosµNEURO Research Centre of Excellence, University of Antwerp, Antwerp, Belgium.
Annemie Van der LindenBio-Imaging Lab, University of Antwerp, Universiteitsplein 1, 2610 Wilrijk, Antwerp, Belgium.
Marleen VerhoyeBio-Imaging Lab, University of Antwerp, Universiteitsplein 1, 2610 Wilrijk, Antwerp, Belgium.
University of Antwerp · BECHDI Foundation · USInserm · FRLeiden University Medical Center · NL

Funding

CHDI Foundation A-15040Fonds Wetenschappelijk Onderzoek I000123NFonds Wetenschappelijk Onderzoek I003420NFonds Wetenschappelijk Onderzoek OZ3544
6 · The paper itself

Abstract

backgroundHuntington's disease (HD) is marked by a CAG-repeat expansion in the huntingtin gene that causes neuronal dysfunction and loss, affecting mainly the striatum and the cortex. Alterations in the neurovascular coupling system have been shown to lead to dysregulated energy supply to brain regions in several neurological diseases, including HD, which could potentially trigger the process of neurodegeneration. In particular, it has been observed in cross-sectional human HD studies that vascular alterations are associated to impaired cerebral blood flow (CBF). To assess whether whole-brain changes in CBF are present and follow a pattern of progression, we investigated both resting-state brain perfusion and vascular reactivity longitudinally in the zQ175DN mouse model of HD.

methodsUsing pseudo-continuous arterial spin labelling (pCASL) MRI in the zQ175DN model of HD and age-matched wild-type (WT) mice, we assessed whole-brain, resting-state perfusion at 3, 6 and 9 and 13 months of age, and assessed hypercapnia-induced cerebrovascular reactivity (CVR), at 4.5, 6, 9 and 15 months of age.

resultsWe found increased perfusion in cortical regions of zQ175DN HET mice at 3 months of age, and a reduction of this anomaly at 6 and 9 months, ages at which behavioural deficits have been reported. On the other hand, under hypercapnia, CBF was reduced in zQ175DN HET mice as compared to the WT: for multiple brain regions at 6 months of age, for only somatosensory and retrosplenial cortices at 9 months of age, and brain-wide by 15 months. CVR impairments in cortical regions, the thalamus and globus pallidus were observed in zQ175DN HET mice at 9 months, with whole brain reactivity diminished at 15 months of age. Interestingly, blood vessel density was increased in the motor cortex at 3 months, while average vessel length was reduced in the lateral portion of the caudate putamen at 6 months of age.

conclusionOur findings reveal early cortical resting-state hyperperfusion and impaired CVR at ages that present motor anomalies in this HD model, suggesting that further characterization of brain perfusion alterations in animal models is warranted as a potential therapeutic target in HD.

Indexed as

Huntington DiseaseAnimalsBrainCross-Sectional StudiesDisease Models, AnimalHumansHypercapniaInfantMicePerfusionBlood vesselsBrain perfusionCerebral blood flowCerebrovascular reactivityHuntington’s disease

Identifiers

PMID38627751
PMCPMC11022401
OpenAlexW4394838420

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.