Abstract

AbstractBackgroundThe association between ApoE e4, a powerful genetic risk factor for AD, and beta‐amyloid (Aβ) pathology has been reported, but the evidence for the correlation with tau pathology is not as clear. The current study examined the relationship between ApoE e4 allele and plasma concentrations of p‐tau181 in patients with clinically diagnosed AD compared with an age‐matched controls with normal cognitive function.MethodWe examined 302 EDTA plasma samples of patients assessed at the UBC Hospital Clinic for Alzheimer’s disease. The cohort was clinically characterized as controls (n = 59) if no significant cognitive impairment was found, and AD (n = 243) if they fulfilled the NIA‐AA criteria (McKhann 2011). The plasma ptau‐181 levels were measured using an ADx‐developed p‐tau181‐specific Simoa assay. ApoE genotyping was performed on extracted DNA from blood samples. We examined the association of presence of ApoE e4 allele and plasma p‐tau181 concentrations using two‐by‐two ANOVA using SPSS 29.ResultThe plasma concentrations of p‐tau181 in AD who are ApoE e4 carriers (75.4 pg/ml) were slightly higher than but not significantly different from in AD non‐ ApoE4 carriers (70.1 pg/ml) (p = 0.64). The plasma levels of ptau‐181 in control cases with and without the ApoE allele were 24.8 and 24 pg/ml respectively (p = 1.000). There was no statistical significant interaction between the effects of AD and ApoE e4 carrier status on plasma p‐tau181 (F (1, 298) = 0.21, p = 0.65, ηp2 = 0.001).ConclusionWhile the plasma p‐tau181 concentrations were significantly higher in AD groups compared to controls (p<0.001) it was no significant effect of ApoE e4 genotype on the levels of plasma p‐tau181 in the control or AD groups (p = 0.94, p = 0.21). This suggests that the ApoE e4 carrier status does not affect plasma p‐tau181 concentrations significantly, independent of the AD clinical status.

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