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@ARTICLE{PrezMillan:283183,
author = {Pérez-Millan, Agnès and Falgàs, Neus and Bosch, Beatriz
and Borrego-Écija, Sergi and Antonell, Anna and
Fernández-Villullas, Guadalupe and Esteller-Gauxax, Diana
and Tort-Merino, Adrià and Bargalló, Núria and Balasa,
Mircea and Lladó, Albert and Aguillon, David and Chrem,
Patricio and Day, Gregory S and Devenney, Emma and Huey,
Edward D and Ikeuchi, Takeshi and Jucker, Mathias and
Kasuga, Kensaku and Vöglein, Jonathan and Roh, Jee Hoon and
Vitali, Paolo and Sosa Ortiz, Ana Luisa and Llibre-Guerra,
Jorge J and Gordon, Brian A and McDade, Eric and Bateman,
Randall J and Sánchez-Valle, Raquel},
collaboration = {Network, Dominantly Inherited Alzheimer},
othercontributors = {Bateman, Randall and Daniels, Alisha J and Courtney, Laura
and Ziegemeier, Angela and Skrbec, Karina and Hellm,
Cortaiga and Martin, Mariana and Ziegemeier, Ellen and
Bartzel, Jamie and McDade, Eric and Llibre-Guerra, Jorge J
and Supnet-Bell, Charlene and Xiong, Chengie and Xu, Xiong
and Lu, Ruijin and Wang, Guoqiao and Li, Yan and Nie,
Yuzheng and Gremminger, Emily and Perrin, Richard J and
Franklin, Erin and Ibanez, Laura and Jerome, Gina and
Stauber, Jennifer and Baker, Bryce and Minton, Matthew and
Cruchaga, Carlos and Goate, Alison M and Renton, Alan E and
Picarello, Danielle M and Fulton-Howard, Brian and
Benzinger, Tammie L S and Gordon, Brian A and Banks, Jessica
and Hornbeck, Russ and Chen, Allison and Chen, Charles and
Flores, Shaney and Goyal, Manu and Hobbs, Diana and
Joseph-Mathurin, Nelly and Jackson, Kelley and Keefe, Sarah
and Koudelis, Deborah and Massoumzadeh, Parinaz and
McCullough, Austin and McKay, Nicole and Nicklaus, Joyce and
Pulizos, Christine and Wang, Qing and Sabaredzovic, Edita
and Scott, Jalen and Simmons, Ashlee and Rizzo, Jacqueline
and Vlassenko, Andrei and Wang, Yong and Hassenstab, Jason
and Smith, Jennifer and Stout, Sarah and Aschenbrenner,
Andrew J and Karch, Celeste M and Marsh, Jacob and Morris,
John C and Holtzman, David M and Barthélemy, Nicolas R and
Xu, Jinbin and Berman, Sarah B and Ikonomovic, Snezana and
Day, Gregory S and Graff-Radford, Neill R and Farlow, Martin
and Chhatwal, Jasmeer P and Maa, Courtney and Ikeuchi,
Takeshi and Kasuga, Kensaku and Ishiguro, Takanobu and
Ishii, Kenji and Senda, Michio and Niimi, Yoshiki and Huey,
Edward D and Salloway, Stephen and Devenney, Emma and
Schofield, Peter R and Brooks, William S and Bechara, Jacob
A and Martins, Ralph and Fox, Nick C and Cash, David M and
Ryan, Natalie S and Jucker, Mathias and Laske, Christoph and
Timofejavaite, Reda and Kuder-Buletta, Elke and
Gräber-Sultan, Susanne and la Fougère, Christian and
Reischl, Gerald and Obermueller, Ulrike and Levin, Johannes
and Rödenbeck, Yvonne and Vöglein, Jonathan and Lee,
Jae-Hong and Roh, Jee Hoon and Vitali, Paolo and Allegri,
Ricardo F and Mendez, Patricio Chrem and Surace, Ezequiel
and Vazquez, Silvia and Aguillon, David and Leon, Yudy
Milena and Ramirez, Laura and Serna, Laura and Baena, Ana
and Bocanegra, Yamile and Levey, Allan I and Johnson, Erik C
B and Seyfried, Nicholas T and Ringman, John and Fagan, Anne
M and Mori, Hiroshi and Masters, Colin and Noble, James M
and Sanchez-Valle, Raquel and Lopera, Francisco},
title = {{C}ortical asymmetry in autosomal dominant {A}lzheimer's
disease progression.},
journal = {Brain communications},
volume = {8},
number = {1},
issn = {2632-1297},
address = {[Oxford]},
publisher = {Oxford University Press},
reportid = {DZNE-2026-00062},
pages = {fcaf488},
year = {2026},
abstract = {The cortical asymmetry index evaluates the cortical
thickness asymmetry between hemispheres. We investigated
cortical asymmetry index in asymptomatic and symptomatic
mutation carriers of autosomal dominant Alzheimer's disease
to explore the brain asymmetry within the Alzheimer's
disease continuum. Sixty baseline T1-weighted MRI scans were
obtained from the Clinic Barcelona cohort. Baseline and
longitudinal MRI data from 564 participants within the
dominantly inherited Alzheimer network observational study
were used as an independent, confirmatory cohort.
Cerebrospinal fluid and plasma neurofilament light chain
levels were included when available. Cortical thickness was
calculated using Freesurfer and cortical asymmetry index was
calculated via an open-source pipeline. Cross-sectional
analyses examined cortical asymmetry index differences based
on clinical classification and APOE ε4 status, adjusting
for age, sex and estimated years from onset, while
correlations were assessed with age, estimated years from
onset, mini-mental state examination scores, and
neurofilament light. Longitudinal cortical asymmetry index
evolution was modelled using generalized additive models in
the dominantly inherited Alzheimer network observational
study cohort, incorporating age, sex, and the interaction
between group and estimated years from onset. The cortical
asymmetry index successfully distinguished asymptomatic
mutation carrier and symptomatic mutation carriers from
healthy controls in the Clinic Barcelona cohort and
symptomatic mutation carriers from controls in dominantly
inherited Alzheimer network observational study. Higher
cortical asymmetry index in mutation carriers (asymptomatic
mutation carrier and symptomatic mutation carriers combined)
and in symptomatic mutation carriers were associated with
higher plasma neurofilament light levels, a closer proximity
to symptom onset, and lower mini-mental state examination in
the Clinic Barcelona cohort. In the dominantly inherited
Alzheimer network observational study cohort, mutation
carriers exhibited increased cortical asymmetry index
compared to controls and correlated with elevated
neurofilament light (plasma and Cerebrospinal fluid), lower
mini-mental state examination, and a closer proximity to
symptom onset. APOE3/3 carriers showed greater asymmetry
than other APOE genotypes and significant cortical asymmetry
index differences between asymptomatic mutation carrier and
symptomatic mutation carriers. Longitudinally, cortical
asymmetry index increased over time significantly in
symptomatic mutation carriers. These findings underscore
brain asymmetry as a potential biomarker for early
Alzheimer's disease progression in autosomal dominant
Alzheimer's disease, with implications for detection and
monitoring tracking disease-related neuroanatomical
changes.},
keywords = {APOE (Other) / Alzheimer’s disease (Other) / autosomal
dominant Alzheimer’s disease (Other) / brain (Other) /
magnetic resonance imaging (Other)},
cin = {AG Jucker / Clinical Research (Munich)},
ddc = {610},
cid = {I:(DE-2719)1210001 / I:(DE-2719)1111015},
pnm = {352 - Disease Mechanisms (POF4-352) / 353 - Clinical and
Health Care Research (POF4-353)},
pid = {G:(DE-HGF)POF4-352 / G:(DE-HGF)POF4-353},
experiment = {EXP:(DE-2719)DIAN-20090101},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:41523185},
pmc = {pmc:PMC12781868},
doi = {10.1093/braincomms/fcaf488},
url = {https://pub.dzne.de/record/283183},
}
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