Alzheimer's disease Animal Model by Aluminum, Beta-Amyloid and Transforming Growth Factor Beta-1

Alzheimer's disease (AD) is a chronic, progressing neuronal degeneration disease, However, the etiology and pathogenesis of AD is not clear. In order to be helpful in understanding the etiology and pathogenesis of AD, a new multi-factors rat model of AD was designed, which could closely mimic the distinctive changes of praxiology, pathology and molecularbiology in this study. Aβ1-40 and aluminum into the lateral cerebral ventricle and transforming growth factor beta-1(TGFβ-1) into the anterodorsal nucleus of thalamus were stereotaxically injected. The praxiological disorders were examined by hematoxylin and eosin ( HE ), Congo red and silver staining, and choline acetyl transferase ( ChAT ) and Aβ were measured by immunohistochemistry. The results showed that the cognitive ability of the model rats was damaged, neurons became derangement and karyopyknosis, moreover, senile plaques ( SP ) and neurofibrillary tangles ( NFTs ) were found in the cortex and hippocampus over 3 months, choline acetyl transferase was decreased, and Aβ was increased. All of these changes could persist longer than 3 months.