In 132 community-dwelling older adults, higher beat-to-beat systolic blood pressure variability measured by continuous monitoring tracked with higher plasma p-Tau217 (β=0.32, p=0.008), p-Tau181 (β=0.22, p=0.05) and GFAP (β=0.41, p=0.00001), after adjustment for age, sex, systolic pressure and APOE4 status. No association appeared with the amyloid-β42/40 ratio or neurofilament light. The pattern points toward tau and astrocyte-reactivity pathways rather than amyloid retention.
The tau-and-GFAP signal matters because most prior BPV work used visit-to-visit readings, which blend true physiology with medication adherence, white-coat effects and measurement noise. Beat-to-beat data sidestep much of that, hinting that autonomic or vascular stiffness mechanisms, not just treatment behavior, drive the link. Still, the design is cross-sectional, so reverse causation is plausible: early Alzheimer's pathology could impair autonomic regulation and raise variability. The sample is small, recruited from the community, and the p-Tau181 result sits right at the significance threshold. The abstract does not say whether antihypertensive use or multiple-comparison correction were handled. Practically, adults cannot yet act on beat-to-beat variability, and no evidence shows that lowering it reduces dementia risk. This preprint has not been peer reviewed, so findings may shift. Editorially, it is incremental and confirmatory, reinforcing blood pressure instability as a dementia-relevant marker and justifying longitudinal and interventional follow-up.