CI showed variable degrees

of CI, which included the clinical diagnoses of amnestic MCI (n = 1) (Petersen 2004), possible AD (n = 1), probable AD (n = 2), demented (n = 1), and mixed vascular dementia and AD (n = 1) at the time of death. All individuals in the CI group had moderate NP (CERAD score B), Braak scores ranging from II to V, and received a neuropathologic diagnosis of possible (N = 1, subject with MCI) or probable AD (n = 6) by CERAD criteria. There were no significant differences in the number of years of education (CI 16.0 SD 2.4, ASYMAD 17.7 SD 2.9, and CN 16.1 SD 4.1) or baseline Primary Mental AG 14699 Ability Test (PMA) Vocabulary Test Inhibitors,research,lifescience,medical score (CI 33.7 SD 11.0, ASYMAD 39.9 SD 2.9, and CN 38.6 SD Inhibitors,research,lifescience,medical 7.0) among the three groups. On the tests used to determine clinical diagnosis, there were no baseline (year 1) differences between the groups. When examining the annual rates of change in performance, the BMS (P = 0.006), Boston Naming (P = 0.03), and Trails B (P = 0.006) tests showed overall group differences. Follow-up comparisons revealed that the

CI group showed greater decline than the CN group on the Boston Naming task (P = 0.01), and greater decline than both CN and ASYMAD groups on the Trails B test (P’s < 0.03). The ASYMAD group, although still considered CN, showed greater decline than the CI group on the BMS exam (P = 0.002). The last available CDR scale Inhibitors,research,lifescience,medical scores were obtained on average 11 months (range 1–30 months) prior

to death and were significantly greater in the CI group than the ASYMAD (P < 0.005) and CN groups (P < 0.05). There were no significant differences between the groups in the number of individuals who were positive Inhibitors,research,lifescience,medical for the APOE e4 allele, as both CI and ASYMAD groups had two individuals with an APOE genotype of 3/4. There were also no differences in the number of individuals with history of hypertension, smoking, or diabetes during the study. Table 3 shows the semiquantitative neuropathologic assessment of CERAD and Braak scores. The Inhibitors,research,lifescience,medical CI and ASYMAD groups had identical CERAD NP scores (all subjects CERAD out age-related plaque score B). The CN group had less NP pathology than both the ASYMAD and CN groups. The majority of CN subjects (n = 6) had no NP, while one subject had sparse NP (CERAD age related plaque score A). There was no difference in Braak scores among the three groups. Stereology Two subjects in the CN group did not have adequate material to perform quantitative stereology on the MTG. For all other areas (MFG, IP, precuneus) material was available from all 19 subjects. The CI and ASYMAD groups showed no significant difference in amyloid (both neuritic and diffuse plaques) in the MFG and IP. CI had greater β-amyloid in the PreCu and MTG (P < 0.05) than both CN and ASYMAD. ASYMAD and CI had more β-amyloid than CN in MFG, PreCu, and IP (P≤ 0.05).