Evidence map›Paper›PMID 40473890›Full record

ArticleScientific reports2025

Brain lateralization for perceiving direction of motion is reversed in Williams syndrome and related to BUD23.

Debra L Mills, Li Dai, Julie R Korenberg

Abstract read
In one paragraph

Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

3 authors.

Debra L MillsSchool of Psychology and Sport Science, Bangor University, Bangor, UK. d.l.mills@bangor.ac.uk.
Li DaiDepartment of Pediatrics, University of Utah, Salt Lake City, UT, USA.
Julie R KorenbergDepartment of Pediatrics, University of Utah, Salt Lake City, UT, USA. julie.korenberg@hsc.utah.edu.

Funding

Williams Syndrome: The Molecular Genetic CharacterizationP01HD033113 · NICHD · UNIVERSITY OF UTAH · PI KORENBERG, JULIE RUTH · 1996 to 2015
$19.4M
Leverhulme Trust IAF-2018-014National Institute of Child Health and Human Development 3P01HD033113-12S1A1NICHD NIH HHS P01 HD033113
6 · The paper itself

Abstract

Lateralized nervous system function is phylogenetically old but fundamentally important for human brain function. Although altered in developmental and psychiatric disorders, we know little about its genetics. To understand the genetic origins of hemispheric specialization, we investigated laterality in a genetic disorder, Williams Syndrome (WS), caused by ~ 27 deleted genes on 7q11.2. Using a multidisciplinary approach combining individuals' molecular genetic, electrophysiological, and behavioral data, we identify reversed lateralization, from right to left hemisphere for perceiving direction of motion in WS and show hemispheric strengths are inversely correlated. Moreover, we correlate decreased transcript levels of the deleted gene BUD23, with strength of the reversed lateralization and with decreased performance in mental rotation, another right hemisphere lateralized function. The results implicate dosed BUD23, an 18S ribosomal RNA methyltransferase, in human brain laterality, support an evolutionary origin and provide altered lateralization as a novel mechanism for impaired cognition in genetic and behavioral disorders.

Indexed as

BrainFunctional LateralityMethyltransferasesMotion PerceptionWilliams SyndromeAdolescentAdultFemaleHumansMaleYoung AdultMethyltransferases

Identifiers

PMID40473890
PMCPMC12141689

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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.