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@ARTICLE{Lohner:296171,
author = {V. Lohner and L. Perna and B. Schöttker$^*$ and R.
Perneczky and M. Kliegel and H. Brenner$^*$ and U. Mons},
title = {{A}ssociations of biomarkers of neurodegenerative diseases
with mild neurocognitive disorder in a cohort of patients
with stable coronary heart disease},
journal = {Alzheimer's and dementia},
volume = {20 Suppl 8},
issn = {1552-5260},
address = {Hoboken, NJ},
publisher = {Wiley},
reportid = {DKFZ-2025-00098},
pages = {e095214},
year = {2024},
note = {Developing Topics: Poster presentation},
abstract = {Coronary heart disease (CHD) is a well-known risk factor
for cognitive impairment and dementia, and blood biomarkers
of neurodegenerative diseases may be utilised to identify
people at higher risk of cognitive decline. Here, we aimed
to investigate prospective associations between these
biomarkers and mild neurocognitive disorder (MiND) after a
follow-up of ten years in patients with stable CHD, and
potential effect modification by hypercholesterolemia and
ApoE genotype.Biomarkers of neurodegenerative diseases
(glial fibrillary acidic protein (GFAP), neurofilament light
chain (NfL), and phosphorylated tau181 (p-tau181)) were
measured in baseline blood serum samples using the
Single-Molecule Array (Simoa) Technology (Quanterix, USA) in
a subset (n = 363) of a cohort of patients with stable CHD.
MiND was defined as scores ≤ 21.8 on the Cognitive
Telephone Screening Instrument (COGTEL).
Hypercholesterolemia was categorised into none (normal total
cholesterol (TC) levels without statin use), normal TC
levels with statin use, or increased TC levels independent
of statin use. We evaluated prospective associations of
biomarkers of neurodegenerative disease with MiND using
multivariable logistic regression models, adjusted for age,
sex, study centre, hearing impairment, and comorbidities. We
additionally checked for biomarker×ApoE genotype and
biomarker×hypercholesterolemia interactions.At follow-up,
55 $(15.2\%)$ patients had developed MiND. Higher levels of
NfL were associated with increased risks of developing MiND
(OR $(95\%-CI)$ per SD increase: 1.44 (1.01-2.04)).
Associations of p-tau181 with MiND were depending on
hypercholesterolemia, but not on ApoE genotype. Higher
levels of p-tau181 were associated with lower odds of
developing MiND in patients without hypercholesterolemia (OR
$(95\%-CI)$ per SD increase: 0.09 (0.01-0.39)) and higher
odds of developing MiND in patients with increased TC levels
(OR $(95\%-CI)$ per SD increase: 7.83 (1.72-103.20)), but
not in patients with normal TC levels using statins. Levels
of GFAP were not associated with MiND.Preliminary analyses
suggest that NfL and p-tau181 predict MiND after ten years
in patients with stable CHD, and that the association of
p-tau181 with MiND was modified by hypercholesterolemia.
This might imply that a deterioration in cognitive
performance in this population might be halted through early
management of hypercholesterolemia, however, more research
is warranted.},
subtyp = {Other},
keywords = {Humans / Male / Female / Aged / Biomarkers: blood / tau
Proteins: blood / Cognitive Dysfunction: blood / Coronary
Disease: blood / Hypercholesterolemia: blood / Glial
Fibrillary Acidic Protein: blood / Prospective Studies /
Middle Aged / Neurofilament Proteins: blood /
Apolipoproteins E: genetics / Risk Factors / Genotype /
Biomarkers (NLM Chemicals) / tau Proteins (NLM Chemicals) /
Glial Fibrillary Acidic Protein (NLM Chemicals) /
Neurofilament Proteins (NLM Chemicals) / neurofilament
protein L (NLM Chemicals) / Apolipoproteins E (NLM
Chemicals)},
cin = {C070},
ddc = {610},
cid = {I:(DE-He78)C070-20160331},
pnm = {313 - Krebsrisikofaktoren und Prävention (POF4-313)},
pid = {G:(DE-HGF)POF4-313},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:39783714},
doi = {DOI:10.1002/alz.095214},
url = {https://inrepo02.dkfz.de/record/296171},
}