A total of 323 homebound elderly individuals from the NAME study were used for this study analysis. These participants came to the hospital to have a brain MRI and had the data on the brain infarct subtypes and the ApoE4 allele.13
In total, 8% (n = 27) had LV infarcts, 18% (n = 60) had SV infarcts, and 2% (n = 8) had both LV and SV infarcts on brain MRI (). The average age of this study sample was 73.3 ± 8.3 (mean ± SD) years old, and 73% were females. The sample was multiethnic with 62% white, 35% African American, and 3% other ethnicities. In total, 76% of the participants completed a high school education or above.
Of the homebound elderly individuals, 25% participants were ApoE4 carriers (n = 80). We first examined whether there was an association between ApoE4 allele and the infarct subtypes. shows that there were no differences in the demographic information except ethnicity between those with and without ApoE4 allele. The numbers of cases with either infarct subtypes in addition to the peripheral vascular diseases including cardiovascular disease, diabetes, and hypertension in those with and without ApoE4 allele did not show statistical differences. We compared the serum activities of Aβ-degrading proteases between the ApoE4 carriers and ApoE4 noncarriers. Again, there were no differences of substrate V degradation, ACE N-domain, and ACE C-domain activities between the presence and the absence of ApoE4.
Demographic and Medical Status of Nonapolipoprotein E4 Alleleand Apolipoprotein E4 Carriers in the Homebound Elderly Populationa
We then studied whether there were associations between the infarct subtypes and the Aβ-degrading activities in blood. Using the multivariate linear regression model, serum substrate V degradation as an outcome was positively associated with the number of SV infarcts (β = +.031, SE = 0.013, P = .02), but not with of SV infarcts, (β = +.031, SE = 0.013, P = .02), but not with the number of LV infarcts, after adjusting for age, sex, ethnicity, BMI, and the ApoE4 allele (). Adding the vascular diseases into the model did not affect these relationships (Model II). Although there were high percentages of diabetes (32%), taking aspirin (42%) and statin (45%) in the homebound elderly population, these variables were not associated with substrate V degradation and did not affect the relationship between SV infarcts and substrate V degradation in serum (data not shown).
Linear Multivariable-Adjusted Correlates of Substrate V Degradation as an Outcome and Each Infarct Subtypea
Further, we found that serum substrate V degradation as an outcome was significantly associated with the interaction between ApoE4 and the number of SV infarcts (β = +.158, SE = 0.034, P < .0001; (model III in ), but not the interaction between ApoE4 and the number of LV infarcts (data not shown). Consistently, the association between increased substrate V degradation and the number of SV infarcts was only found among the ApoE4 carriers (β = +.154, SE = 0.031, P < .0001), but not among the ApoE4 non-carriers (β = +.001, SE = 0.014, P = .94; ). In the presence of ApoE4, the higher the number of SV infarcts, the higher the average serum activity of substrate V degradation (Mean ± SD: no SV infarct = 0.90 ± 0.14, 1 SV infarct = 0.99 ± 0.09, and more than 1 SV infarct = 1.67 ± 0.35, P = .004; ). In the absence of ApoE4, there was no difference in substrate V degradation between those with and without SV infarcts. When ACE N-terminal- and C-terminal-specific substrates were also used, we did not find any associations between the ACE activities and SV infarcts regardless of the ApoE4 genotype.
Linear Multivariable-Adjusted Correlates of Substrate V Degradation as an Outcome and Each Infarct Subtype Among Those Apolipoprotein E4 Allele Carriers Versus Noncarriers
Comparisons of Substrate V Degradation Versus ACE-Specific Activities in Different Infarct Subgroupsa