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@ARTICLE{Franzmeier:155552,
author = {Franzmeier, Nicolai and Ossenkoppele, Rik and Brendel,
Matthias and Rubinski, Anna and Smith, Ruben and Kumar, Atul
and Mattsson-Carlgren, Niklas and Strandberg, Olof and
Duering, Marco and Bürger, Katharina and Dichgans, Martin
and Hansson, Oskar and Ewers, Michael and Initiative, ,
Alzheimer's Disease Neuroimaging and study, the Swedish
BioFINDER},
title = {{T}he {BIN}1 rs744373 {A}lzheimer's disease risk {SNP} is
associated with faster {A}β-associated tau accumulation and
cognitive decline.},
journal = {Alzheimer's and dementia},
volume = {18},
number = {1},
issn = {1552-5279},
address = {Hoboken, NJ},
publisher = {Wiley},
reportid = {DZNE-2021-00730},
pages = {103-115},
year = {2022},
abstract = {The BIN1 rs744373 single nucleotide polymorphism (SNP) is a
key genetic risk locus for Alzheimer's disease (AD)
associated with tau pathology. Because tau typically
accumulates in response to amyloid beta (Aβ), we tested
whether BIN1 rs744373 accelerates Aβ-related tau
accumulation.We included two samples (Alzheimer's Disease
Neuroimaging Initiative [ADNI], n = 153; Biomarkers for
Identifying Neurodegenerative Disorders Early and Reliably
[BioFINDER], n = 63) with longitudinal 18 F-Flortaucipir
positron emission tomography (PET), Aβ biomarkers, and
longitudinal cognitive assessments. We assessed whether BIN1
rs744373 was associated with faster tau-PET accumulation at
a given level of Aβ and whether faster BIN1
rs744373-associated tau-PET accumulation mediated cognitive
decline.BIN1 rs744373 risk-allele carriers showed faster
global tau-PET accumulation (ADNI/BioFINDER,
P < .001/P < .001). We found significant Aβ by rs744373
interactions on global tau-PET change (ADNI: β/standard
error [SE] = 0.42/0.14, P = 0.002; BioFINDER:
β/SE = -0.35/0.15, P = .021), BIN1 risk-allele carriers
showed accelerated tau-PET accumulation at higher Aβ
levels. In ADNI, rs744373 effects on cognitive decline were
mediated by faster global tau-PET accumulation
(β/SE = 0.20/0.07, P = .005).BIN1-associated AD risk is
potentially driven by accelerated tau accumulation in the
face of Aβ.},
keywords = {Adaptor Proteins, Signal Transducing: genetics / Aged /
Alzheimer Disease: genetics / Amyloid beta-Peptides:
cerebrospinal fluid / Amyloid beta-Peptides: metabolism /
Biomarkers: cerebrospinal fluid / Brain: metabolism /
Cognitive Dysfunction: metabolism / Female / Humans / Male /
Nuclear Proteins: genetics / Polymorphism, Single Nucleotide
/ Positron-Emission Tomography / Tumor Suppressor Proteins:
genetics / tau Proteins: metabolism / Alzheimer's disease
(Other) / BIN1 (Other) / amyloid (Other) / tau (Other)},
cin = {AG Höglinger 2 / AG Simons},
ddc = {610},
cid = {I:(DE-2719)1111015 / I:(DE-2719)1110008},
pnm = {351 - Brain Function (POF4-351) / 353 - Clinical and Health
Care Research (POF4-353)},
pid = {G:(DE-HGF)POF4-351 / G:(DE-HGF)POF4-353},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:34060233},
doi = {10.1002/alz.12371},
url = {https://pub.dzne.de/record/155552},
}