ArticleFrontiers in aging neuroscience2025
Amyloid pathology modulates the relationship between subsyndromal symptomatic depression and tau accumulation in non-demented older adults.
Article in Frontiers in aging neuroscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Objective: Subsyndromal symptomatic depression (SSD) has been increasingly implicated in the pathophysiological processes of Alzheimer's disease (AD). However, it remains unclear whether SSD and amyloid-β (Aβ) pathology jointly contribute to tau deposition. This study aimed to investigate the interaction between SSD and Aβ status on regional tau accumulation in non-demented older adults. Materials and methods: We analyzed data from 391 non-demented older adults in the Alzheimer's Disease Neuroimaging Initiative (ADNI) who underwent Aβ and tau positron emission tomography (PET) scans, as well as Geriatric Depression Scale (GDS-15) assessments. Aβ positivity (Aβ+) was defined by established tracer-specific standardized uptake value ratio (SUVR) thresholds (≥1.11 for Results: At baseline, significant interactions between SSD and Aβ status were observed for regional tau SUVRs, with the Aβ+/SSD+ group exhibiting significantly higher tau levels across all Braak stages compared with the other groups. Longitudinal analyses identified a significant three-way interaction among SSD, Aβ status, and time in the Braak III/IV and Braak V/VI regions. Moreover, the Aβ+/SSD+ group demonstrated significantly faster tau accumulation compared to all other groups. The Aβ+/SSD- group also exhibited greater tau accumulation than the Aβ-/SSD- group, whereas no significant differences were observed between the Aβ- groups. Conclusion: These findings suggest that SSD is associated with greater early tau accumulation in individuals with Aβ pathology.
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