001). In contrast, scores for both cored and diffuse SP for each region (except for diffuse SP in occipital cortex: X2 = 11.7, P = 0.008) did not significantly differ across the four pathological phenotypes (cored-frontal: X2 = 1.8, P = 0.609; temporal: X2 = 3.5, P = 0.318; occipital: X2 = 7.1, P = 0.07) (diffuse-frontal: X2 = 2.4, P = 0.495; temporal: X2 = 2.2, P = 0.534). Post-hoc analysis for diffuse SP in occipital cortex revealed a significant difference between group 1 and group

2 (P < 0.001). There were no significant differences between the four groups with regard to the proportion selleck products of patients with ‘typical’ vs. ‘focal’ variants of AD. A statistically significant (X2 = 4.1, P = 0.042) difference in gender proportions was observed between group 1 and group 2 (Figure 3) such that women (64.7%) made up a greater proportion of group 1 than men, but a lesser proportion of group 2 (43.4%). There were no statistically significant differences in the distribution of cases with a positive family history PD-L1 inhibitor of AD across the four pathological phenotypes.

There were no significant differences between the four pathological phenotypes for either the mean age of onset (F3,96 = 1.248, P = 0.297), mean age at death (F3,117 = 1.364, P = 0.257), mean disease duration (F3,97 = 11.786, P = 0.277) or mean brain weight (F3,111 = 0.370, P = 0.775) (Table 1). The frequency of APOE alleles and genotype within each pathological phenotypic group are shown in Table 2. There was a statistically significant difference between the genotype groups with the ε4/ε4 genotype frequency being significantly higher in group 3 compared with group

1 (χ2 = 9.6, P = 0.002) and the ε3/ε3 genotype frequency consequently being significantly lower in group 3 compared with group 1 (χ2 = 4.5, P = 0.033). The APOE ε4 allele frequency was significantly higher in group 3 than group 1 χ2 = 9.7, P = 0.002), but only tended to be higher in group 2 compared with group 3 χ2 = 3.6, P = 0.057). No significant differences in ε2 allele frequency were found between any of the four pathological groups. Seven cases were identified where the pathological phenotype was not clearly assignable, although these most closely resembled the type 2 phenotype (Table 3). All had Aβ deposition in the form of numerous Unoprostone SP and CAA in leptomeningeal and cortical vessels which, while present in the frontal and/or temporal lobe, and in contrast to ‘typical’ type 2 cases, was NOT present within the occipital lobe. No significant differences were seen in either the age of onset (P = 0.716), age at death (P = 0.930), disease duration (P = 0.630) or brain weight (P = 0.952) were found between these and the typical group 2 cases. There was no significant difference in the proportion of APOE ε4 allele bearers between the typical group 2 cases and the group 2 ‘outliers’.