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. 2024 May 29;20(7):4389–4400. doi: 10.1002/alz.13800

TABLE 4.

Relationships between change in SBP (systolic blood pressure) and change in CSF biomarkers in three study subgroups (n = 191).

Normotension

(n = 125)

Controlled hypertension

(n = 34)

Uncontrolled hypertension

(n = 32)

Log T‐tau 0.001 (−0.001 to 0.003), p = 0.34 −0.001 (−0.005 to 0.003), p = 0.76 0.004 (0.007 to0.002), p  = 0.001
T‐tau 0.51 (−0.16 to 1.17), p = 0.14 −0.50 (−1.71 to 0.71), p = 0.41 1.03 (1.76 to (0.30), p  = 0.01
Log P‐tau 181 −0.001 (−0.003 to 0.001), p = 0.22 0.000 (−0.003 to 0.003), p = 0.99 −0.002 (−0.005 to 0.000), p = 0.03
P‐tau 181 −0.07 (−0.16 to 0.02), p = 0.13 0.03 (−0.14 to 0.20), p = 0.71 −0.11 (−0.22 to −0.01), p = 0.03
Aβ42 −0.35 (−1.96 to 1.25), p = 0.67 −0.94 (−3.82 to 1.94), p = 0.52 −0.39 (−2.21 to 1.44), p = 0.68

Note: Respective p values for slopes (change in biomarker with changes in SBP) are derived from mixed models for repeated measures. Biomarker was a dependent variable and SBP, group, and group × SBP interaction were predictors. Age at baseline was added as covariate in all models. Parentheses indicate 95% CI for slopes. Due to adjustment for multiple comparisons, slopes were considered significantly different from 0 at p < 0.016 (bolded in table). The group × SBP interaction term for both log transformed and untransformed T‐tau was p = 0.009.