Abstract: Objective To investigate expression of β-site APP-cleaving enzymel(BACE1) and Aβ in brain of diabetes mellitus of Wistar rats，to study pathophysiological mechanism of Alzheimer disease from diabetic metabolic disorder. Methods Animal model of diabetes mellitus was established by streptozocin with intraperitoneal injection. Wistar rats were randomly divided into normal group (N), sham-operation group (S), 4 weeks diabetes mellitus model group (M4), 6 weeks diabetes mellitus model group (M6) and 8 weeks diabetes mellitus model group (M8). Behaviour was tested with Morris water maze and shuttle box test. Expression of Aβ was measured by enzyme linked immunosorbent assay and BACE1 by immunohistochemistry, enzyme linked immunosorbent assay, Western blotting and RT-PCR. The absorbance value was measured by imaging analysis. Results The electric times and latancy of memory and study were more increased in model group than that in N and S group but the times of escape more decreased(EM>P/EM><0.01). The expression of Aβ1SUB>40/SUB> increased from (64.13±6.76)pg/mg in normal group to (86.43±7.03)pg/mg in model group by ELISA(EM>P/EM><0.001) and Aβ1SUB>42/SUB> from (67.43±5.12 )pg/mg in normal group to (89.45±5.28) pg/mg (EM>P/EM><0.001) in model group. The expression of BACE1 increased from (116.46±8.10)pg/mg in normal group to (158.73±6.24)pg/mg in model group by ELISA and from 0.61±0.11 in normal group to 1.52±0.16 by Western blotting absorbance valule and from 1.62±0.26 in normal group to 3.61±0.32 by RT-PCR absorbance valule and from 0.81±0.21 in normal group to 2.01±0.36 by immunohistochemistry absorbance valule (EM>P/EM><0.001). The expr

Key words: Diabetes mellitus, β-amyloid precursor protein cleavage enzyme 1, β-amyloid protein, ELISA, Western blotting, RT-RCR, Rat