A Study Of The Correlation Between Alzheimer’s Disease And The Expression Of THR α1in Rats Brain Tissues

Objective:To study the correlation between Alzheimer’s disease (AD) and the expression of thyroid receptor al (THR al) in brain tissues by establishing a rat model of AD, and therefore to investigate its mechanism primarily from the angle of phosphorylation of protein tau aggravated by the over-expression of THR al.Methods:D-galactose (50mg·kg-1·d-1) was administered by intraperitoneal injection into SD rats from AD group, while equal amount of saline into that from control group. After six weeks’ administration,these rats were observed mental state, activities, etc. Tissues from the whole brain were made into pathological sections by the secondary fixed, whose morphological changes were then observed under optical microscope. The differential expression of mRNA encoding THR al, CDK-5, p35and that of protein pser404-tau were determined using real time fluorescence quantitative PCR and Western-blot respectively.Results:Compared with control group, AD rats were dull appearance and slow reaction., the neurons of cerebral cortex and hippocampus in particular from AD group were disorganized, with their nuclei hyperchromatic、pyknosis, their axons hyperchromatic, trailing, and formed the neurons fiber tangles.The amount of expression of THRα1、CDK-5and p35mRNA increased, were1.20±0.30、4.71±0.54、2.11±0.40with statistical significance(P<0.05); while in the same time, in hippocampal, the amount of expression of them were2.53±0.65、18.51±2.77、5.96±0.49respectively with statistical significance (P<0.05)。And the amount of pser404-tau protein is significantly higher than that of the rats in the control group(P<0.05).Conclusion:The expression of mRNA encoding THR al in neurons of cerebral cortex and hippocampus from AD group is significantly higher than control group. Over-expression of THR al can increase the expression of mRNA encoding protein phosphorylation related kinase, namely CDK-5. And it in turn aggravates the phosphorylation of protein tau in neurons, which may participate or contribute to the pathological process of AD.