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@ARTICLE{Roe:1021979,
author = {Roe, James M and Vidal-Pineiro, Didac and Amlien, Inge K
and Pan, Mengyu and Sneve, Markus H and Thiebaut de
Schotten, Michel and Friedrich, Patrick and Sha, Zhiqiang
and Francks, Clyde and Eilertsen, Espen M and Wang, Yunpeng
and Walhovd, Kristine B and Fjell, Anders M and
Westerhausen, René},
title = {{T}racing the development and lifespan change of
population-level structural asymmetry in the cerebral
cortex},
journal = {eLife},
volume = {12},
issn = {2050-084X},
address = {Cambridge},
publisher = {eLife Sciences Publications},
reportid = {FZJ-2024-01118},
pages = {e84685},
year = {2023},
abstract = {Cortical asymmetry is a ubiquitous feature of brain
organization that is subtly altered in some
neurodevelopmental disorders, yet we lack knowledge of how
its development proceeds across life in health. Achieving
consensus on the precise cortical asymmetries in humans is
necessary to uncover the developmental timing of asymmetry
and the extent to which it arises through genetic and later
influences in childhood. Here, we delineate population-level
asymmetry in cortical thickness and surface area vertex-wise
in seven datasets and chart asymmetry trajectories
longitudinally across life (4–89 years; observations =
3937; $70\%$ longitudinal). We find replicable asymmetry
interrelationships, heritability maps, and test asymmetry
associations in large–scale data. Cortical asymmetry was
robust across datasets. Whereas areal asymmetry is
predominantly stable across life, thickness asymmetry grows
in childhood and peaks in early adulthood. Areal asymmetry
is low-moderately heritable (max h2SNP $~19\%)$ and
correlates phenotypically and genetically in specific
regions, indicating coordinated development of asymmetries
partly through genes. In contrast, thickness asymmetry is
globally interrelated across the cortex in a pattern
suggesting highly left-lateralized individuals tend towards
left-lateralization also in population-level
right-asymmetric regions (and vice versa), and exhibits low
or absent heritability. We find less areal asymmetry in the
most consistently lateralized region in humans associates
with subtly lower cognitive ability, and confirm small
handedness and sex effects. Results suggest areal asymmetry
is developmentally stable and arises early in life through
genetic but mainly subject-specific stochastic effects,
whereas childhood developmental growth shapes thickness
asymmetry and may lead to directional variability of global
thickness lateralization in the population.},
cin = {INM-7},
ddc = {600},
cid = {I:(DE-Juel1)INM-7-20090406},
pnm = {5251 - Multilevel Brain Organization and Variability
(POF4-525)},
pid = {G:(DE-HGF)POF4-5251},
typ = {PUB:(DE-HGF)16},
pubmed = {37335613},
UT = {WOS:001070991900001},
doi = {10.7554/eLife.84685},
url = {https://juser.fz-juelich.de/record/1021979},
}