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. 2025 Aug 22;105(6):e214024. doi: 10.1212/WNL.0000000000214024

Table 3.

Associations of Aβ With CAA When Examined Without or With the 4 CAA-Related Proteins

Source of Aβ Series Model terms Associations with CAA: estimate (SE), p value
SMOC1 SFRP1 APOE APOE4
Aβ load, a pathologic measure (A) Aβ and the proteins are examined in separate models Aβ load 0.830 (0.086), <0.001 0.818 (0.088), <0.001 0.830 (0.086), <0.001 0.849 (0.087), <0.001
Protein 1.552 (0.135), <0.001 2.018 (0.224), <0.001 1.797 (0.220), <0.001 0.412 (0.052), <0.001
(B) Each model includes Aβ and one of the proteins Aβ load 0.246 (0.121), 0.042 0.669 (0.091), <0.001 0.741 (0.087), <0.001 0.725 (0.089), <0.001
Protein 1.281 (0.188), <0.001 1.586 (0.225), <0.001 1.484 (0.222), <0.001 0.302 (0.053), <0.001
Total Aβ protein, a proteomic measure (A) Aβ and the proteins are examined in separate models Total Aβ protein 0.249 (0.023), <0.001 0.247 (0.024), <0.001 0.249 (0.023), <0.001 0.249 (0.024), <0.001
Protein 1.499 (0.139), <0.001 2.033 (0.237), <0.001 1.810 (0.228), <0.001 0.394 (0.053), <0.001
(B) Each model includes Aβ and one of the proteins Total Aβ protein 0.142 (0.032), <0.001 0.212 (0.025), <0.001 0.218 (0.024), <0.001 0.221 (0.024), <0.001
Protein 0.904 (0.192), <0.001 1.539 (0.239), <0.001 1.295 (0.231), <0.001 0.265 (0.055), <0.001
Aβ38 peptide, a proteomic measure (A) Aβ and the proteins are examined in separate models Aβ38 0.559 (0.061), <0.001 0.557 (0.061), <0.001 0.559 (0.061), <0.001 0.558 (0.061), <0.001
Protein 1.498 (0.139), <0.001 2.031 (0.237), <0.001 1.805 (0.227), <0.001 0.393 (0.053), <0.001
(B) Each model includes Aβ and one of the proteins Aβ38 0.486 (0.062), <0.001 0.507 (0.063), <0.001 0.464 (0.064), <0.001 0.543 (0.061), <0.001
Protein 1.363 (0.141), <0.001 1.857 (0.245), <0.001 1.293 (0.248), <0.001 0.380 (0.054), <0.001

Abbreviations: Aβ = β-amyloid; CAA = cerebral amyloid angiopathy; SFRP1 = secreted frizzled-related protein 1; SMOC1 = secreted modular calcium-binding protein 1.

In a series of ordinal logistic regression models, we examined the associations of 3 measures of Aβ (Aβ load, derived from immunohistochemical assessment of brain sections; total Aβ protein and Aβ38 peptide, both derived from proteomic analysis of 20 mg of the dorsolateral prefrontal cortex) with CAA without (series-A) and with (series-B) the 4 CAA-related proteins in the models. In each model CAA was the outcome, and model terms were one of the Aβ measures alone (series-A) or with (series-B) one of the 4 proteins listed in the right columns. All the models were controlled for age at death and sex. The analyses indicated that the associations of 2 of the Aβ measures (Aβ load and total Aβ proteins) with CAA were attenuated when SMOC1 was in the model.