Table 1 Neuropathological staging of AD was confirmed using H & E, silver, amyloid and p-Tau staining, which included Braak and CERAD stages as shown in Table 1 All EOAD cases, with the exception of one, had a Braak stage of V-VI and a CERAD plaque stage of C (definite AD). LOAD cases were Braak V-VI and a CERAD of C, except for two cases; one had a Braak stage of V-VI and a CERAD of 0-A and a second had Braak stage of VI and a CERAD of B. For the DS cases, all except two DS-MCI cases had a Braak of VI and a CERAD stage of C (definite AD). However, the two DS-MCI cases had significant accumulation of both NFTs and plaques with Braak III-IV and IV-V, respectively and both were a CERAD of C. Finally, the control cases (aged 42–100 years) had a Braak stage of 0-III with CERAD staging of 0-B. The 100-year-old case had a CERAD plaque density of C and was excluded due to the high plaque count, leaving an N of 8 in that group. Importantly, examination of the clinical records of the nine control cases revealed reports of cognitive impairment. Most of the control cases (7 out of 9) originated from the Medical University of South California (MUSC) brain bank, where a full medical history was available. The fetal DS and control tissues were obtained from University of Zagreb without information other than the gestational week, gender, and DS vs. normosomic status. The average post-mortem interval (PMI) was significantly higher (p = 0.019) for the control cases (5.75–25 h) compared to DS cases (one-way ANOVA: F_2,16 = 4.729, p = 0.024). However, no significant differences in PMI were observed between DS-AD and AD. No correlations between PMI and outcome measures (PIB, THK5117, Amylo-glo or AT8) were found suggesting that PMI was not acting as a covariate

From: Regional binding of tau and amyloid PET tracers in Down syndrome autopsy brain tissue