Dissociation of tau pathology and neuronal hypometabolism within the ATN framework of Alzheimer's disease.
Where this comes from
- Record sourced from PubMed, PMID 35314672.
- Also identified by DOI 10.1038/s41467-022-28941-1 and PMC identifier 8938426.
- Licence recorded as CC BY.
- The licence permits redistribution, so the abstract is shown in full and the full text is available from the publisher.
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 <sup>18</sup>F-flortaucipir vs. <sup>18</sup>F-fluorodeoxyglucose positron emission tomography as markers of T and neuronal hypometabolism (N<sub>M</sub>) in 289 symptomatic patients from the Alzheimer's Disease Neuroimaging Initiative. We identified six T/N<sub>M</sub> clusters with differing limbic and cortical patterns. The canonical group was defined as the T/N<sub>M</sub> 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/N<sub>M</sub> mismatch reveals distinct imaging signatures with pathobiological and prognostic implications for AD.
Medical subject headings
- Alzheimer Disease
- Cognitive Dysfunction