[Study of the correlation about IGF-I receptor and β-amyloid in Alzheimer's disease]

To detect the expression of IGF-I receptor in the hippocampus neuron of rat treated by Aβ(1-42), and thus from the receptor level explore the disorder of central nervous insulin signaling and the possible molecular mechanism of Alzheimer disease.

Cultured primary hippocampus neurons were treated with different concentrations of Aβ(1-42), apoptosis rate was detected by flow cytometry, real-time quantitative PCR and Western blot were used to detect IGF-I receptor expression.

Primary cultured cells mature in 7(th) days; after detected by flow cytometry, early apoptosis rate in Aβ(1-42) 0, 30, 60, 100 µmol/L groups showed a concentration-dependent increase. PCR results showed that, in 30 (1.72 ± 0.33) and 60 µmol/L (1.86 ± 0.36) treatment groups levels of the IGF-I receptor gene were significantly higher than the control group (regarded as 1) (P < 0.01), 100 µmol/L group (0.70 ± 0.15) was significantly lower than the control group (P < 0.05). Results of Western blot showed 30 and 60 µmol/L protein level of the treatment groups are 1.08 ± 0.04, 1.74 ± 0.08 (P < 0.01) and 100 µmol/L group was 0.79 ± 0.11(P < 0.05), which had same trend with PCR.

Aβ(1-42) induced altered expression of IGF-I receptors in rat hippocampus cells, maybe one of the molecule mechanisms of Alzheimer disease.