Objective      To determine the distribution and expression of amylin in the brain of Alzheimer’s disease (AD) model mice

ob/ob mice (obese mice) and wild-type controls for the relationship between amylin and senile plaques

so as to investigate whether amylin is involved in the pathogenesis of senile dementia.       Methods      Five-month-old APP/PS1 double transgenic male mice (AD model)

ob/ob mice and the wild-type mice were employed in this study. Immunofluorescence assay was used to detect the distribution and expression of amylin and senile plaques in the brain of 3 groups of mice.       Results      Amylin was widely distributed and expressed in the neurons throughout almost all the regions of brain in the APP/PS1 double transgenic mice

including the cerebral cortex

hippocampus

dorsal thalamus

and so on

with very high levels in the insular cortex and piriform cortex (P＜0.01). While senile plaques were selectively distributed in the cerebral cortex and hippocampus. The distribution of amylin was much more extensive than that of senile plaques in the brain of the AD mice. Amylin positive substances were found gathering around the deposition of senile plaques. The number of amylin-positive neurons in the cerebral cortex was significantly higher in the AD and ob/ob mice than that the wild-type mice (P＜0.05

P＜0.01).       Conclusion      The distribution and expression of amylin are obviously different in the brain of the AD

ob/ob and wild-type mice

and these differences may promote the formation of senile plaques and be involved in the pathogenesis of AD.