HAI Book 2025 - Flipbook - Page 117
Bischof, Gerard
7
Molecular correlates of apraxia in Alzheimer's disease: A PET imaging
study
Gerard Bischof1,2, Elena Jaeger1,2, Kathrin Giehl1,2, Frank jessen3,4, Oezguer Onur5,6, Sid
O9Bryant7,8, Esra Kara3, Peter Weiss6, Alexander Drzezga1,2
1
University of Cologne, University Hospital of Cologne, Department of Nuclear Medicine, Multimodal Neuroimaging
Group, Cologne, Germany, Cologne, DE
2
Research Center Juelich, Institute for Neuroscience and Medicine II, Molecular Organization of the Brain, Juelich,
Germany, Juelich, DE
3
University of Cologne, University Hospital of Cologne, Department of Psychiatry, Cologne, Germany, Cologne, DE
4
German Center for Neurodegenerative Diseases, Bonn/Cologne, Germany, Cologne, DE
5
University of Cologne, University Hospital of Cologne, Department of Neurology, Cologne, Germany, Cologne, DE
6
Research Center Juelich, Institute for Neuroscience and Medicine III, Cognitive Neuroscience, Juelich, Germany,
Juelich, DE
7
Institute for Translational Research University of North Texas Health Science Center Fort Worth Texas USA., Fort
Worth, TX, US
8
Department of Family Medicine, Texas College of Osteopathic Medicine, University of North Texas Health Science
Center, Fort Worth, Texas USA, Fort Worth, TX, US
Apraxia is a prominent symptom of Alzheimer9s disease (AD), yet the mechanisms driving this behavioral trait
remain poorly understood. In this study, we aimed to systematically investigate apraxia profiles in AD patients and
explore potential links to tau pathology using the second-generation tau PET tracer [18F]PI-2620. We
hypothesized that distinct patterns of tau deposition in the brain might underlie the apraxic deficits observed in
AD.
We recruited a cohort of 32 patients with confirmed AD and a control group of 41 cognitively unimpaired
individuals (CU1). Apraxia was assessed in all participants using the Dementia Apraxia Screening Test (DATE) and
the Cologne Apraxia Screening (KAS). AD patients also underwent PET imaging with [18F]PI-2620 to map tau
pathology. To further examine the relationship between apraxia and tau deposition, we compared the PET data
from AD patients with a separate group of 54 amyloid-negative, cognitively unimpaired individuals (CU2). Z-score
deviation maps were generated, and voxel-based multiple regression analysis was performed.
Our findings revealed significant clusters of tau accumulation in regions associated with apraxia, including the
angular gyrus, as well as temporal, parietal, and lateral occipital cortical areas. These areas correlated strongly
with apraxia severity and were consistent across both apraxia assessment tools. In contrast, no significant
correlations were found between tau uptake in primary motor or subcortical brain regions and apraxia.
These results suggest that tau deposition in specific cortical regions may lead to localized neuronal dysfunction,
which in turn results in apraxic impairments in a dose-dependent manner. This study offers new insights into the
relationship between tau pathology and the manifestation of apraxia in AD, advancing our understanding of the
neural mechanisms underlying this complex symptom.
Keywords: Apraxia, 18F-PI2620, Alzheimer’s Disease, Tau
HAI2025 - 117
