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@INPROCEEDINGS{Behrenbruch:283097,
author = {Behrenbruch, Niklas and Schwarck, Svenja and
Schumann-Werner, Beate and Molloy, Eóin N. and Hochkeppler,
Anne and Buechel, Anna-Therese and Moyano, Jose Bernal and
Incesoy, Enise I and Garcia-Garcia, Berta and Vockert,
Niklas and Marcos Morgado, Barbara and Fischer, Larissa and
Müller, Patrick and Behnisch, Gusalija and Seidenbecher,
Constanze I and Schott, Björn H and Esselmann, Hermann and
Wiltfang, Jens and Barthel, Henryk and Sabri, Osama and
Kreissl, Michael C and Düzel, Emrah and Maass, Anne},
title = {{L}ifestyle and health signatures of brain pathological and
cognitive aging},
journal = {Alzheimer's and dementia},
volume = {21},
number = {Suppl 8},
issn = {1552-5260},
reportid = {DZNE-2025-01504},
pages = {e109741},
year = {2025},
abstract = {While aging almost inevitably leads to some degree of
cognitive decline, the interindividual heterogeneity in the
trajectories of decline raises the question of the extent to
which resistance against pathology and cognitive resilience
are involved. Using a multimodal approach including
neuroimaging, fitness assessment, questionnaire data, and
Alzheimer's disease (AD) genetic risk and plasma biomarkers
(Figure 1), we aimed to characterize latent structures of
lifestyle, mental and bodily health, estimate indices of
brain (pathological) and cognitive aging, and relate
lifestyle/health profiles and AD genetic risk to these
indices.We analyzed a subsample of 211 cognitively normal
older adults aged ≥ 60 years from an ongoing study
(CRC1436) (age=71.0±7.4years, $46\%$ female). Using
principal component analysis, we derived seven principal
components (PCs) that capture latent structures of lifestyle
and general health from thirty variables (Figure 2B). To
characterize successful brain/cognitive aging, we calculated
a brain (BAG) and cognitive age gap (CAG) as the difference
between brain pathology-/cognition-predicted age and
chronological age (Figure 2A). Our novel BAG estimate
incorporated also AD pathology, white matter
hyperintensities and enlarged perivascular spaces. We
regressed the first seven principal components (PC) on BAG
and CAG to estimate the association of lifestyle/health
profiles with successful brain/cognitive aging. We further
assessed whether APOE4 carriers had higher BAG/CAG using a
two-sample t-test.We named the PCs according to their main
factor loadings (Figure 2B). PC1 (Low Mental Health), PC2
(Active Life), and PC5 (Mentally Inactive $\&$ Physically
Active) were significantly associated with CAG, whereas only
PC2 was significantly associated with BAG (Figure 3A). BAG
partly explained the relationship between PC2 and CAG
(partial mediation of $18.0\%$ of total effect, p = 0.027;
Figure 3B). Finally, APOE e4 carrier had significantly
higher BAG (p = 0.049), but not CAG (p = 0.155).Our results
suggest that factors of cognitive resilience and brain
maintenance are to some extent unified in an active
lifestyle described by physical fitness, mental leisure
activities, and lower cardiovascular risk. In addition,
engagement in mental leisure activities may explain
cognitive resilience independent of brain pathology.
Finally, genetic risk for AD may also accelerate brain aging
in cognitively healthy older adults.},
month = {Jul},
date = {2025-07-27},
organization = {Alzheimer’s Association
International Conference, Toronto
(Canada), 27 Jul 2025 - 31 Jul 2025},
keywords = {Humans / Female / Aged / Male / Alzheimer Disease: genetics
/ Alzheimer Disease: pathology / Alzheimer Disease:
diagnostic imaging / Brain: pathology / Brain: diagnostic
imaging / Middle Aged / Life Style / Magnetic Resonance
Imaging / Aging: pathology / Principal Component Analysis /
Aged, 80 and over / Neuroimaging / Biomarkers: blood /
Biomarkers (NLM Chemicals)},
cin = {AG Maaß / AG Düzel / AG Müller / AG Fischer / AG
Wiltfang / Core MR PET},
ddc = {610},
cid = {I:(DE-2719)1311001 / I:(DE-2719)5000006 /
I:(DE-2719)1310003 / I:(DE-2719)1410002 / I:(DE-2719)1410006
/ I:(DE-2719)1340016},
pnm = {353 - Clinical and Health Care Research (POF4-353) / 352 -
Disease Mechanisms (POF4-352)},
pid = {G:(DE-HGF)POF4-353 / G:(DE-HGF)POF4-352},
typ = {PUB:(DE-HGF)1 / PUB:(DE-HGF)16},
pubmed = {pmid:41433525},
pmc = {pmc:PMC12724826},
doi = {10.1002/alz70862_109741},
url = {https://pub.dzne.de/record/283097},
}