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@ARTICLE{Schroeter:972038,
author = {Schroeter, Matthias L. and Godulla, Jannis and Thiel,
Friederike and Taskin, Birol and Beutner, Frank and Dubovoy,
Vladimir K. and Teren, Andrej and Camilleri, Julia and
Eickhoff, Simon and Villringer, Arno and Mueller, Karsten},
title = {{H}eart failure decouples the precuneus in interaction with
social cognition and executive functions},
journal = {Scientific reports},
volume = {13},
number = {1},
issn = {2045-2322},
address = {[London]},
publisher = {Macmillan Publishers Limited, part of Springer Nature},
reportid = {FZJ-2023-01047},
pages = {1236},
year = {2023},
abstract = {Aging increases the risk to develop Alzheimer's disease.
Cardiovascular diseases might accelerate this process. Our
study aimed at investigating the impact of heart failure on
brain connectivity using functional magnetic resonance
imaging at resting state. Here we show brain connectivity
alterations related to heart failure and cognitive
performance. Heart failure decreases brain connectivity in
the precuneus. Precuneus dysconnectivity was associated with
biomarkers of heart failure-left ventricular ejection
fraction and N-terminal prohormone of brain natriuretic
peptide-and cognitive performance, predominantly executive
function. Meta-analytical data-mining approaches-conducted
in the BrainMap and Neurosynth databases-revealed that
social and executive cognitive functions are mainly
associated with those neural networks. Remarkably, the
precuneus, as identified in our study in a mid-life cohort,
represents one central functional hub affected by
Alzheimer's disease. A long-term follow-up investigation in
our cohort after approximately nine years revealed more
severe cognitive impairment in the group with heart failure
than controls, where social cognition was the cognitive
domain mainly affected, and not memory such as in
Alzheimer's disease. In sum, our results indicate
consistently an association between heart failure and
decoupling of the precuneus from other brain regions being
associated with social and executive functions. Further
longitudinal studies are warranted elucidating
etiopathological mechanisms.},
cin = {INM-7},
ddc = {600},
cid = {I:(DE-Juel1)INM-7-20090406},
pnm = {5252 - Brain Dysfunction and Plasticity (POF4-525)},
pid = {G:(DE-HGF)POF4-5252},
typ = {PUB:(DE-HGF)16},
pubmed = {36690723},
UT = {WOS:000954571900022},
doi = {10.1038/s41598-023-28338-0},
url = {https://juser.fz-juelich.de/record/972038},
}