Fig. 6

Enhanced Aβ₄₂-α7nAChR association by plasma from APOEε4 carriers with MCI or dementia due to AD correlates with longitudinal cognitive decline. Rat frontal cortical synaptosomes were incubated simultaneously with 25 μl plasma and 0.1 μM Aβ₄₂. The levels of Aβ₄₂-α7nAChR complexes were determined by the abundance of α7nAChRs in the anti-Aβ₄₂ antibody immunoprecipitates by Western blotting (a), quantified by densitometric scanning, and normalized by β-actin immunoreactivity as the immunoprecipitation/loading controls. The data expressed as the ratios of positive plasma to negative plasma (mean ± SEM) summarizes the effects of plasma derived from two separate visits on Aβ₄₂-elicited the Aβ₄₂-α7nAChR association in different diagnostic groups without b and with c segregating by the APOE genotype. *p < 0.01, **p < 0.05, compared to respective cognitive normal group b or APOE ε2/ε3 c by Dunnett’s test adjusted for multiple comparisons. d Correlation to baseline cognitive status defined by Mini-Mental State Examination (MMSE) score (n = 86): spearman correlation coefficient, controls = 0.19 (–0.23; 0.55); MCI = –0.32 (–0.61; 0.06); AD = –0.14 (–0.46; 0.22); all = –0.71 (–0.80; –0.59). e Correlation to longitudinal cognitive changes per evolution of diagnostic group (control not progressed (CTRL NP) and progressed (P), MCI NP and P, and AD): spearman correlation coefficient controls NP = –0.19 (–0.58; 0.26); controls P = NA; MCI NP = –0.19 (–0.67; 0.40); MCI P = –0.22 (–0.64; 0.31); AD = –0.30 (–0.58; 0.05); all = –0.57 (–0.70; –0.41). α7nAChR α7-nicotinic acetylcholine receptor, Aβ amyloid beta, AD Alzheimer’s disease, apoE apolipoprotein, C controls, MCI mild cognitive impairment, V visit