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Table 2 Associations between global WMH and AD and WMH risk factors

From: Spatial patterns of white matter hyperintensities associated with Alzheimer’s disease risk factors in a cognitively healthy middle-aged cohort

  Model 1 (Direct) Model 2 (Age-corrected) Model 3 (Hypertension-corrected)
Effect size (95% CI) p Effect size (95% CI) p Effect size (95% CI) p
CAIDE-I 0.11 (0.03 to 0.19) 0.017 0.01 (−0.07 to 0.09) 0.423 0.01 (−0.08 to 0.09) 0.444
Age 0.22 (0.13 to 0.29) < 0.001 0.18 (0.09 to 0.26) < 0.001
Hypertension 0.14 (0.05 to 0.22) < 0.001 0.09 (0.00 to 0.17) 0.017
Hypercholesterolemia 0.09 (0.00 to 0.17) 0.042 0.05 (−0.04 to 0.14) 0.207 0.07 (−0.02 to 0.15) 0.051
BMI 0.08 (−0.00 to 0.16) 0.053 0.06 (−0.02 to 0.14) 0.207 0.03 (−0.05 to 0.11) 0.249
Sex (Men) −0.01 (−0.09 to 0.08) 0.411 −0.01 (−0.10 to 0.07) 0.423 −0.03 (−0.11 to 0.05) 0.246
Education −0.04 (−0.13 to 0.04) 0.192 −0.01 (−0.09 to 0.08) 0.423 −0.02 (−0.11 to 0.06) 0.313
Physical exercise −0.04 (−0.13 to 0.04) 0.192 −0.05 (−0.14 to 0.03) 0.207 −0.02 (−0.10 to 0.07) 0.352
Maternal family history of AD* 0.12 (−0.02 to 0.17) 0.077 0.12 (0.03 to 0.21) 0.024 0.08 (−0.01 to 0.18) 0.040
APOE-ε2/ε3* −0.13 (−0.24 to -0.01) 0.042 −0.08 (−0.20 to 0.04) 0.2077 −0.10 (−0.21 to 0.02) 0.054
  1. The three models had WMH/TIV (%) as an outcome variable; no covariates were used in Model 1; age effect was corrected for in Model 2 and hypertension was accounted for in Model 3
  2. Significant results are shown in bold (p < 0.05, false discovery ratio-corrected)
  3. Participants without a family history of AD and APOE-ε3 homozygotes were the reference group for group comparisons
  4. AD Alzheimer’s disease, APOE apolipoprotein E, BMI body mass index, CAIDE Cardiovascular Risk Factors, Aging, and Incidence of Dementia, CI confidence interval, TIV total intracranial volume, WMH white matter hyperintensities
  5. *All other pairwise group comparisons showed no significant associations and are not shown in the table
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