Dissociation of tau pathology and neuronal hypometabolism within the ATN framework of Alzheimer’s disease

Michael Tran Duong, Sandhitsu R. Das, Xueying Lyu, Long Xie, Hayley Richardson, Sharon X. Xie, Paul A. Yushkevich, David A. Wolk () and Ilya M. Nasrallah ()
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Michael Tran Duong: University of Pennsylvania
Sandhitsu R. Das: University of Pennsylvania
Xueying Lyu: University of Pennsylvania
Long Xie: University of Pennsylvania
Hayley Richardson: University of Pennsylvania
Sharon X. Xie: University of Pennsylvania
Paul A. Yushkevich: University of Pennsylvania
David A. Wolk: University of Pennsylvania
Ilya M. Nasrallah: University of Pennsylvania

Nature Communications, 2022, vol. 13, issue 1, 1-15

Abstract: Abstract Alzheimer’s disease (AD) is defined by amyloid (A) and tau (T) pathologies, with T better correlated to neurodegeneration (N). However, T and N have complex regional relationships in part related to non-AD factors that influence N. With machine learning, we assessed heterogeneity in 18F-flortaucipir vs. 18F-fluorodeoxyglucose positron emission tomography as markers of T and neuronal hypometabolism (NM) in 289 symptomatic patients from the Alzheimer’s Disease Neuroimaging Initiative. We identified six T/NM clusters with differing limbic and cortical patterns. The canonical group was defined as the T/NM pattern with lowest regression residuals. Groups resilient to T had less hypometabolism than expected relative to T and displayed better cognition than the canonical group. Groups susceptible to T had more hypometabolism than expected given T and exhibited worse cognitive decline, with imaging and clinical measures concordant with non-AD copathologies. Together, T/NM mismatch reveals distinct imaging signatures with pathobiological and prognostic implications for AD.

Date: 2022
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DOI: 10.1038/s41467-022-28941-1

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