% IMPORTANT: The following is UTF-8 encoded. This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.
@ARTICLE{Bischof:1037233,
author = {Bischof, Gérard N. and Jaeger, Elena and Giehl, Kathrin
and Jessen, Frank and Onur, Oezguer A. and O'Bryant, Sid and
Kara, Esra and Weiss, Peter H. and Drzezga, Alexander},
title = {{C}ortical {T}au {A}ggregation {P}atterns {A}ssociated
{W}ith {A}praxia in {P}atients {W}ith {A}lzheimer {D}isease},
journal = {Neurology},
volume = {103},
number = {12},
issn = {0028-3878},
address = {Philadelphia, Pa.},
publisher = {Wolters Kluwer},
reportid = {FZJ-2025-00566},
pages = {e210062},
year = {2024},
note = {A. Drzezga, G.N. Bischof, E. Jaeger, and P.H. Weiss are
fundedby the Deutsche Forschungsgemeinschaft -
Project-ID431549029 - SFB 1451. G.N. Bischof received
funding fromAlzheimer Forschung Initiative e.V., Germany
(AFI K1707).In addition, this study was supported by the
German ResearchFoundation (DFG, DR 445/9-1). Precursor for
the synthesisof the tracer [18F]PI-2620 was kindly provided
by Life Molecularimaging. The [18F]PI-2620 control sample
was kindlyprovided by SidO’Bryant and were taken from the
HABS-HDdatabase (apps.unthsc.edu/itr/studies/habs).
Researchreported on this publication was supported by the
NationalInstitute on Aging of the NIH under Award
NumbersR01AG054073, R01AG058533, P41EB015922,
andU19AG078109. The content is solely the responsibility of
theauthors and does not necessarily represent the official
views ofthe NIH.},
abstract = {Background and objectives: Apraxia is a frequently observed
symptom in Alzheimer disease (AD), but the causal
pathomechanism underlying this dysfunction is not well
understood. Previous studies have demonstrated associations
between various cognitive dysfunctions in AD and cortical
tau deposition in specific brain areas, suggesting a causal
relationship. Thus, we hypothesized that specific regional
patterns of tau pathology in praxis-related brain regions
may be associated with apraxic deficits in AD. For this
purpose, we performed PET imaging with the second-generation
tau-PET tracer [18F]PI-2620 in a well-defined group of
patients with AD (N = 33) who had been systematically
assessed for apraxia.Methods: Patients with a
biomarker-confirmed diagnosis of AD were recruited in
addition to a sample of cognitively unimpaired (CU1) control
participants. Both groups underwent apraxia assessments with
the Dementia Apraxia Screening Test. In addition, PET
imaging with [18F]PI-2620 was performed to assess tau
pathology in the patients with AD. To specifically
investigate the association of apraxia severity with
regional tau pathology, we compared the PET data from this
group with an independent sample of amyloid-negative
cognitively intact participants (CU2) by generation of
z-score deviation maps and submitted these maps to a
voxel-based multiple regression analysis.Results: A total of
120 participants $(39\%$ female) with a mean age of 67.9
(9.2) years were included in the study (AD = 33; CU1; N =
33; CU2; N = 54). We identified a significant correlation
between circumscribed clusters of tau aggregation in
praxis-related brain regions (including parietal (angular
gyrus), temporal, and occipital regions) and severity of
apraxia in patients with AD. By contrast, no significant
correlations between tau tracer uptake in primary motor
cortex or subcortical brain regions and apraxia were
observed.Discussion: These results suggest that tau
deposition in specific cortical praxis-related brain regions
may induce local neuronal dysfunction leading to a
dose-dependent functional decline in praxis performance in
AD. The awareness of this relationship could further refine
a differentiated individual diagnostic characterization and
classification of patients with AD.},
cin = {INM-3 / INM-2},
ddc = {610},
cid = {I:(DE-Juel1)INM-3-20090406 / I:(DE-Juel1)INM-2-20090406},
pnm = {5251 - Multilevel Brain Organization and Variability
(POF4-525) / DFG project G:(GEPRIS)431549029 - SFB 1451:
Schlüsselmechanismen normaler und krankheitsbedingt
gestörter motorischer Kontrolle (431549029) / 5252 - Brain
Dysfunction and Plasticity (POF4-525) / 5253 - Neuroimaging
(POF4-525)},
pid = {G:(DE-HGF)POF4-5251 / G:(GEPRIS)431549029 /
G:(DE-HGF)POF4-5252 / G:(DE-HGF)POF4-5253},
typ = {PUB:(DE-HGF)16},
pubmed = {39626130},
UT = {WOS:001370437800001},
doi = {10.1212/WNL.0000000000210062},
url = {https://juser.fz-juelich.de/record/1037233},
}