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Fig. 4 | Alzheimer's Research & Therapy

Fig. 4

From: RETRACTED ARTICLE: Increased Aβ42-α7-like nicotinic acetylcholine receptor complex level in lymphocytes is associated with apolipoprotein E4-driven Alzheimer’s disease pathogenesis

Fig. 4

ApoE4 preferentially increases the Aβ42-α7nAChR interaction. Biotin-tagged α7nAChRs trapped streptavidin-coated 96-well plate was incubated with 0.01–100 nM of recombinant apoE subtypes for 10 min prior to addition of 20 nM FITC-conjugated Aβ42. The effect of apoE subtype on the Aβ42-α7nAChRs interaction was determined by the residual FITC signals (a). Rat frontal cortical synaptosomes were incubated with 0.01–10 μM of recombinant apoE subtypes and/or 0.1 μM Aβ42. Synaptosomes were collected by centrifugation, solubilized, and immunoprecipitated with anti-Aβ42 antibodies. The level of Aβ42-associated α7nAChRs in anti-Aβ42 immunoprecipitates was shown by Western blot detection of α7nAChR b and quantified by densitometric scanning (c). *p < 0.01, **p < 0.05, compared to Aβ42 alone by Newman-Keuls multiple comparisons (n = 4–8). α7nAChR α7-nicotinic acetylcholine receptor, amyloid beta, ApoE apolipoprotein E, IP immunoprecipitation

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