ArticleAlzheimer's & dementia : the journal of the Alzheimer's Association2025
Defining the contributions of tau pathology in the amygdala to increasing depressive symptoms in aging.
Article in Alzheimer's & dementia : the journal of the Alzheimer's Association, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
4 citing papers in PubMed.
- Tracking the Continuous Time Dynamics of Tau and Depressive Symptoms across the Alzheimer's Disease Continuum.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- The Amygdala and Politics.Brain sciences · 2026Review
- Dissociable Mechanisms Underlie Differences Between Memory and Metamemory in Older Adults: The Differentiating Role of Anxiety and Depression Symptoms.Hippocampus · 2026Article
- Defining the contributions of tau pathology in the amygdala to increasing depressive symptoms in aging.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
backgroundAmygdala tau accumulates in cognitively normal individuals and may contribute to neuropsychiatric changes.
methodsUsing data from the Alzheimer's Disease Neuroimaging Initiative (ADNI), we investigated relationships among cross-sectional and longitudinal tau ([18F]Flortaucipir [FTP] positron emission tomography), changes in depressive symptoms and memory, and amyloid beta and apolipoprotein E (APOE) ε4 status. We report secondary analyses from the Berkeley Aging Cohort Study (BACS).
resultsLongitudinal increases in depressive symptoms were associated with higher baseline FTP and increasing FTP in the amygdala. Relationships between FTP and depressive symptoms were strongest in APOE ε4 carriers, with moderation effects replicating in BACS. Entorhinal FTP did not show associations with depressive symptoms beyond variance explained by the amygdala but showed some specific associations with memory decline. DISCUSSION: Our findings indicate the strongest coupling between tau accumulation and depressive symptoms in APOE ε4 carriers and reinforce the importance of amygdala tau in understanding neuropsychiatric changes in older adults. HIGHLIGHTS: There is a lack of research focused on the role of tau in the amygdala in cognitively normal older adults. Amygdala tau is related to both worsening depressive symptoms and declining memory performance. APOE ε4 carriers seem to drive positive tau-depressive symptom associations. Focusing on the amygdala tau is useful for understanding neuropsychiatric trajectories in cognitively unimpaired older adults.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.