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@ARTICLE{Sampatakakis:276127,
author = {Sampatakakis, Stefanos N and Mourtzi, Niki and Charisis,
Sokratis and Mamalaki, Eirini and Ntanasi, Eva and
Hatzimanolis, Alex and Ramirez, Alfredo and Lambert,
Jean-Charles and Yannakoulia, Mary and Kosmidis, Mary H and
Dardiotis, Efthimios and Hadjigeorgiou, Georgios and
Megalou, Maria and Sakka, Paraskevi and Scarmeas, Nikolaos},
title = {{W}alking time and genetic predisposition for {A}lzheimer's
disease: {R}esults from the {HELIAD} study.},
journal = {The clinical neuropsychologist},
volume = {39},
number = {1},
issn = {0920-1637},
address = {Abingdon},
publisher = {Routledge, Taylor Francis Group},
reportid = {DZNE-2025-00208},
pages = {83 - 99},
year = {2025},
abstract = {Objective: Our study aimed to explore whether physical
condition might affect the association between genetic
predisposition for Alzheimer's Disease (AD) and AD
incidence. Methods: The sample of participants consisted of
561 community-dwelling adults over 64 years old, without
baseline dementia (508 cognitively normal and 53 with mild
cognitive impairment), deriving from the HELIAD, an ongoing
longitudinal study with follow-up evaluations every 3 years.
Physical condition was assessed at baseline through walking
time (WT), while a Polygenic Risk Score for late onset AD
(PRS-AD) was used to estimate genetic predisposition. The
association between WT and PRS-AD with AD incidence was
evaluated with Cox proportional hazard models adjusted for
age, sex, education years, global cognition score and APOE
ε-4 genotype. Then, the association between WT and AD
incidence was investigated after stratifying participants by
low and high PRS-AD. Finally, we examined the association
between PRS-AD and AD incidence after stratifying
participants by WT. Results: Both WT and PRS-AD were
connected with increased AD incidence (p < 0.05), after
adjustments. In stratified analyses, in the slow WT group
participants with a greater genetic risk had a 2.5-fold
higher risk of developing AD compared to participants with
lower genetic risk (p = 0.047). No association was observed
in the fast WT group or when participants were stratified
based on PRS-AD. Conclusions: Genetic predisposition for AD
is more closely related to AD incidence in the group of
older adults with slow WT. Hence, physical condition might
be a modifier in the relationship of genetic predisposition
with AD incidence.},
keywords = {Humans / Alzheimer Disease: genetics / Alzheimer Disease:
epidemiology / Female / Male / Aged / Genetic Predisposition
to Disease / Longitudinal Studies / Incidence / Cognitive
Dysfunction: genetics / Cognitive Dysfunction:
physiopathology / Aged, 80 and over / Walking: physiology /
Alzheimer’s disease (Other) / genetic predisposition
(Other) / physical condition (Other) / polygenic risk
(Other) / walking time (Other)},
cin = {Patient Studies (Bonn)},
ddc = {610},
cid = {I:(DE-2719)1011101},
pnm = {353 - Clinical and Health Care Research (POF4-353)},
pid = {G:(DE-HGF)POF4-353},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:38741352},
doi = {10.1080/13854046.2024.2344869},
url = {https://pub.dzne.de/record/276127},
}