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@ARTICLE{White:259918,
author = {White, Silke and Mauer, René and Lange, Catharina and
Klimecki, Olga and Huijbers, Willem and Wirth, Miranka},
collaboration = {Initiative, Alzheimer's Disease Neuroimaging},
title = {{T}he effect of plasma cortisol on hippocampal atrophy and
clinical progression in mild cognitive impairment.},
journal = {Alzheimer's $\&$ dementia / Diagnosis, assessment $\&$
disease monitoring},
volume = {15},
number = {3},
issn = {2352-8729},
address = {Hoboken, NJ},
publisher = {Wiley},
reportid = {DZNE-2023-00803},
pages = {e12463},
year = {2023},
abstract = {Both elevated cortisol and hippocampal volume have been
linked to an increased risk for the development of
Alzheimer's disease (AD). This longitudinal study assessed
the effects of plasma cortisol on hippocampal atrophy and
clinical progression rates in patients with mild cognitive
impairment (MCI).Patients with amnestic MCI (n = 304) were
selected from the Alzheimer's Disease Neuroimaging
Initiative (ADNI) based on availability of baseline plasma
cortisol and hippocampal volume measures, assessed at
baseline and during follow-ups. We investigated associations
between plasma cortisol, hippocampal volume, and risk of
clinical progression to AD over a study period of up to 100
months (mean follow-up time 36.8 months) using linear mixed
models, Cox proportional hazards models, and Kaplan-Meier
estimators.Plasma cortisol predicted greater hippocampal
atrophy, such that participants with higher cortisol showed
faster decline in hippocampal volume over time (interaction:
β = -0.15, p = 0.004). Small hippocampal volume predicted a
higher risk of clinical progression to AD (haard ratio [HR]
= 2.15; confidence in terval [CI], 1.64-2.80; p < 0.001). A
similar effect was not found for cortisol (HR = 1.206; CI,
0.82-1.37; p = 0.670) and there was no statistical evidence
for an interaction between hippocampal volume and cortisol
on clinical progression (HR = 0.81; CI, 0.57-0.17; p =
0.260).Our findings suggest that higher cortisol predicts
higher hippocampal atrophy, which in turn is a risk factor
for progression to AD. Regulation of the
hypothalamic-pituitary-adrenal axis through stress-reducing
lifestyle interventions might be a protective factor against
hippocampal degeneration at the prodromal stage of AD.},
keywords = {hypothalamic‐pituitary‐adrenal axis (Other) /
hypothalamic‐pituitary‐adrenal axis (Other) / ADNI
(Other) / MCI (Other) / cortisol (Other) / hippocampus
(Other) / hypothalamic‐pituitary‐adrenal axis (Other) /
neurodegeneration (Other) / risk factor (Other) / stress
(Other)},
cin = {AG Wirth / AG White},
ddc = {610},
cid = {I:(DE-2719)1710011 / I:(DE-2719)1740002},
pnm = {353 - Clinical and Health Care Research (POF4-353)},
pid = {G:(DE-HGF)POF4-353},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:37583892},
pmc = {pmc:PMC10423926},
doi = {10.1002/dad2.12463},
url = {https://pub.dzne.de/record/259918},
}