Evidence map›Paper›PMID 38112342›Full record

ArticleJournal of inherited metabolic disease2024

Quantitative brain morphometry identifies cerebellar, cortical, and subcortical gray and white matter atrophy in late-onset Tay-Sachs disease.

Jitka Májovská, Igor Nestrašil, Alia Ahmed, Monica T Bondy, Jiří Klempíř, Helena Jahnová, Susanne A Schneider, Dana Horáková, Jan Krásenský, Pavel Ješina and 6 more

Open access · hybridAbstract read
In one paragraph

Article in Journal of inherited metabolic disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
2.3field-weighted citation impact, top 10% 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

4 citing papers in PubMed, 4 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 3 countries.

Jitka MájovskáDepartment of Pediatrics and Inherited Metabolic Disorders, First Faculty of Medicine, Charles University and General University Hospital Prague, Prague, Czech Republic.
Igor NestrašilDivision of Clinical Behavioral Neuroscience, Department of Pediatrics, Medical School, University of Minnesota, Minneapolis, Minnesota, USA.
Alia AhmedAdvanced Therapies Program, Division of Genetics and Metabolism, Department of Pediatrics, Medical School, University of Minnesota, Minneapolis, Minnesota, USA.
Monica T BondyDivision of Clinical Behavioral Neuroscience, Department of Pediatrics, Medical School, University of Minnesota, Minneapolis, Minnesota, USA.
Jiří KlempířDepartment of Neurology and Center of Clinical Neuroscience, First Faculty of Medicine, Charles University and General University Hospital in Prague, Prague, Czech Republic.
Helena JahnováDepartment of Pediatrics and Inherited Metabolic Disorders, First Faculty of Medicine, Charles University and General University Hospital Prague, Prague, Czech Republic.
Susanne A SchneiderDepartment of Neurology, LMU University Hospital, LMU Munich, Munich, Germany.
Dana HorákováDepartment of Neurology and Center of Clinical Neuroscience, First Faculty of Medicine, Charles University and General University Hospital in Prague, Prague, Czech Republic.
Jan KrásenskýDepartment of Radiology, First Faculty of Medicine, Charles University and General University Hospital in Prague, Prague, Czech Republic.
Pavel JešinaDepartment of Pediatrics and Inherited Metabolic Disorders, First Faculty of Medicine, Charles University and General University Hospital Prague, Prague, Czech Republic.
Manuela VaneckovaDepartment of Radiology, First Faculty of Medicine, Charles University and General University Hospital in Prague, Prague, Czech Republic.
David R NasceneDepartment of Neuroradiology, Medical School, University of Minnesota, Minneapolis, Minnesota, USA.
Chester B WhitleyAdvanced Therapies Program, Division of Genetics and Metabolism, Department of Pediatrics, Medical School, University of Minnesota, Minneapolis, Minnesota, USA.
Jeanine R JarnesAdvanced Therapies Program, Division of Genetics and Metabolism, Department of Pediatrics, Medical School, University of Minnesota, Minneapolis, Minnesota, USA.
Martin MagnerDepartment of Pediatrics and Inherited Metabolic Disorders, First Faculty of Medicine, Charles University and General University Hospital Prague, Prague, Czech Republic.
Petr DušekDepartment of Neurology and Center of Clinical Neuroscience, First Faculty of Medicine, Charles University and General University Hospital in Prague, Prague, Czech Republic.ORCID 0000-0003-4877-9642
Charles University · CZUniversity of Minnesota · USUniversity of Minnesota Medical Center · USLMU Klinikum · DE

Funding

Training & EducationU54NS065768 · NINDS · UNIVERSITY OF MINNESOTA · PI WHITLEY, CHESTER B. · 2009 to 2024
$17.7M
NINDS NIH HHS U54 NS065768
6 · The paper itself

Abstract

Cerebellar atrophy is a characteristic sign of late-onset Tay-Sachs disease (LOTS). Other structural neuroimaging abnormalities are inconsistently reported. Our study aimed to perform a detailed whole-brain analysis and quantitatively characterize morphometric changes in LOTS patients. Fourteen patients (8 M/6F) with LOTS from three centers were included in this retrospective study. For morphometric brain analyses, we used deformation-based morphometry, voxel-based morphometry, surface-based morphometry, and spatially unbiased cerebellar atlas template. The quantitative whole-brain morphometric analysis confirmed the finding of profound pontocerebellar atrophy with most affected cerebellar lobules V and VI in LOTS patients. Additionally, the atrophy of structures mainly involved in motor control, including bilateral ventral and lateral thalamic nuclei, primary motor and sensory cortex, supplementary motor area, and white matter regions containing corticospinal tract, was present. The atrophy of the right amygdala, hippocampus, and regions of occipital, parietal and temporal white matter was also observed in LOTS patients in contrast with controls (p < 0.05, FWE corrected). Patients with dysarthria and those initially presenting with ataxia had more severe cerebellar atrophy. Our results show predominant impairment of cerebellar regions responsible for speech and hand motor function in LOTS patients. Widespread morphological changes of motor cortical and subcortical regions and tracts in white matter indicate abnormalities in central motor circuits likely coresponsible for impaired speech and motor function.

Indexed as

Tay-Sachs DiseaseWhite MatterAtrophyBrainHumansMagnetic Resonance ImagingRetrospective Studiesbrain atrophyGM2-gangliosidosislate-onset Tay-Sachs diseaseMRI

Identifiers

PMID38112342
PMCPMC10947897
OpenAlexW4389949418

What OpenQuestion holds

Textmetadata
LicenceTDM
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.