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@INPROCEEDINGS{Stark:283068,
author = {Stark, Melina and Kuhn, Elizabeth and Wagner, Michael and
Boecker, Henning and Brosseron, Frederic and Buerger,
Katharina and Daamen, Marcel and Laske, Christoph and
Perneczky, Robert and Peters, Oliver and Priller, Josef and
Schmid, Matthias and Schneider, Anja and Spottke, Annika and
Teipel, Stefan J and Wiltfang, Jens and Düzel, Emrah and
Jessen, Frank and Kleineidam, Luca},
title = {{S}ubjective {C}ognitive {D}ecline and {M}inor
{N}europsychological {D}eficits: {I}mportance for {R}isk
{S}tratification and {T}rial {R}ecruitment in {E}arly
{A}lzheimer´s {D}isease},
journal = {Alzheimer's and dementia},
volume = {21},
number = {Suppl 3},
issn = {1552-5260},
reportid = {DZNE-2025-01475},
pages = {e102815},
year = {2025},
abstract = {The recruitment of participants with a high risk of decline
is crucial for the success of clinical trials in the
earliest phases of Alzheimer´s Disease (AD), where
treatment benefits could be the largest. Subjective
cognitive decline (SCD) and minor neuropsychological
deficits (MNPD) are associated with an increased risk of
cognitive decline, making them promising predictors for this
risk stratification. However, the prognostic value of their
interplay is understudied.We pooled and analyzed data from
cognitively unimpaired participants from the Alzheimer´s
Disease Neuroimaging Initiative (N = 599), DZNE Longitudinal
Cognitive Impairment and Dementia study (N = 618), and
National Alzheimer's Coordinating Center (N = 11,975). SCD
was measured using questionnaires or anamnestic data. MNPD
was defined as a median neuropsychological test performance
of z≤-0.5. We assessed the association of MNPD and SCD
with the conversion to mild cognitive impairment (MCI) and
dementia (cox regression) and baseline amyloid and tau
positivity - measured by PET/CSF (logistic regression). We
adjusted these models for the study cohorts and demographic
covariates. Using power analyses, we calculated the sample
sizes necessary to detect a $30\%$ reduction in the risk of
progressing to MCI over 4.5 years in amyloid positive
participants.In the overall sample (N = 13,192), the
SCD-/MNPD+ (+:present, -:absent; HR=3.13[2.68-3.66]),
SCD+/MNPD- (HR=1.97[1.76-2.20]), and SCD+/MNPD+
(HR=6.23[5.23-7.42]) groups had an increased risk of MCI
compared to the SCD-/MNPD- group. These groups also had an
increased risk of dementia. In amyloid positive participants
(n = 497), this pattern persisted for the progression to
MCI, while only the SCD+/MNPD+ group had an increased risk
for dementia. In participants with biomarker data (n =
2,616), the SCD+/MNPD- (OR=1.47[1.20-1.81]) and SCD+/MNPD+
(OR=1.64[1.04-2.59]) groups had an increased risk of amyloid
positivity. The risk of tau positivity was increased in the
SCD+/MNPD+ group (OR=2.10[1.13-3.90]). In the power
analyses, the required clinical trial size was reduced by
approximately one third after excluding SCD-/MNPD-
individuals and approximately two thirds by focusing only on
SCD+/MNPD+ individuals (Figure).SCD and MNPD have a
complementary prognostic value. SCD+/MNPD+ individuals are
at particularly high risk of pathology and decline. These
clinical symptoms should be taken into account in the
recruitment for clinical trials in preclinical AD.},
month = {Jul},
date = {2025-07-27},
organization = {Alzheimer’s Association
International Conference, Toronto
(Canada), 27 Jul 2025 - 31 Jul 2025},
keywords = {Humans / Male / Female / Aged / Cognitive Dysfunction:
diagnosis / Cognitive Dysfunction: diagnostic imaging /
Cognitive Dysfunction: cerebrospinal fluid / Cognitive
Dysfunction: psychology / Neuropsychological Tests /
Alzheimer Disease: diagnostic imaging / Alzheimer Disease:
diagnosis / Alzheimer Disease: cerebrospinal fluid /
Alzheimer Disease: psychology / tau Proteins: cerebrospinal
fluid / Disease Progression / Longitudinal Studies / Aged,
80 and over / Positron-Emission Tomography / Amyloid
beta-Peptides: cerebrospinal fluid / Biomarkers:
cerebrospinal fluid / tau Proteins (NLM Chemicals) / Amyloid
beta-Peptides (NLM Chemicals) / Biomarkers (NLM Chemicals)},
cin = {AG Wagner / AG Boecker / AG Heneka / Clinical Research
(Munich) / AG Gasser / AG Dichgans / AG Peters / AG Priller
/ AG Schmid Bonn / AG Schneider / AG Spottke / AG Teipel /
AG Wiltfang / AG Düzel / AG Jessen},
ddc = {610},
cid = {I:(DE-2719)1011201 / I:(DE-2719)1011202 /
I:(DE-2719)1011303 / I:(DE-2719)1111015 / I:(DE-2719)1210000
/ I:(DE-2719)5000022 / I:(DE-2719)5000000 /
I:(DE-2719)5000007 / I:(DE-2719)1013028 / I:(DE-2719)1011305
/ I:(DE-2719)1011103 / I:(DE-2719)1510100 /
I:(DE-2719)1410006 / I:(DE-2719)5000006 /
I:(DE-2719)1011102},
pnm = {353 - Clinical and Health Care Research (POF4-353)},
pid = {G:(DE-HGF)POF4-353},
typ = {PUB:(DE-HGF)1 / PUB:(DE-HGF)16},
pubmed = {pmid:41447391},
pmc = {pmc:PMC12740029},
doi = {10.1002/alz70857_102815},
url = {https://pub.dzne.de/record/283068},
}