- Midlife vitamin D linked to tau, not amyloid: Higher 25(OH)D was consistently associated with lower global and AD-vulnerable regional tau burden, but showed no relationship with amyloid-PET.
- Preclinical window matters: Associations were observed in asymptomatic, dementia-free individuals, supporting a potential early-life window for modifying neurodegenerative risk.
- Continuous signal, not threshold: Associations were seen with continuous vitamin D levels, while dichotomous cutoffs (≥30 vs <30 ng/mL) were not significant in fully adjusted models.
- Robust to adjustments: Findings persisted after controlling for vascular risk factors, depression, season, and in sensitivity analyses excluding supplement users.
- Hypothesis-generating, not causal: Results suggest vitamin D as a potentially modifiable factor for tau pathology, but require confirmation in longitudinal cohorts and clinical trials.
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