## 4 Discussion  
The results from this study demonstrated that mice were exposed to Pb for most of their life cycle to construct a mouse model of AD-like lesions, which is in line with the disease spectrum characteristics of Pb as an accumulated poison leading to the development of AD. Based on the successful establishment of a mouse model of AD-like lesions caused by chronic Pb exposure, this study further explored the possible upstream and downstream pathways and modes of action of CDR1 as regulation. There are still many limitations in this study. The set mode of exposure was gastrointestinal, but the exposure mode of practitioners in the actual workplace was mainly respiratory intake. Lack of specific indicators to observe the progression of AD in the course of long-term intoxication, as well as failure to observe the dynamic trend of CDR1 as in the course of chronic intoxication. A growing amount of evidence has confirmed that Pb causes multiple system disorders, with CNS being the top target in acute or chronic Pb exposure. Epidemiological evidence indicates that low-dose Pb exposure for a long period can cause a decline in spatial learning and memory abilities, especially in high-exposed occupational groups [2]. Blood Pb level is an important indicator reflecting the degree of damage and for clinical diagnosis of Pb poisoning. It was found that blood Pb levels of 1.98 \(\mathrm{\SIUnitSymbolMicro g}/\mathrm{dL}\) to 2.02 \(\mathrm{\SIUnitSymbolMicro g}/\mathrm{dL}\) in mice were associated with neurobehavioral abnormalities, such as reduced olfactory recognition and exploratory activity, decreased memory, learning ability, and intelligence [27; 28]. In our study, the blood and hippocampal Pb levels in the Pb-exposed group were significantly higher than those in the control group, especially in the 4 g/L Pb-exposed group, which showed an order-of-magnitude increase in blood and hippocampal Pb levels, suggesting that the mice in the Pb-exposed group were undergoing a higher Pb-loading state and suffering from Pb-neuro Toxicity damage. It was also found that mice in the Pb-exposed group were less active compared to the control group, which had previously shown the same behavior after Pb exposure for 3 months, suggesting that the effect became more pronounced with increasing concentration and time. In another in vivo study, the spatial learning and memory abilities of mice were tested by neurobehavioral tests after being exposed to different concentrations of gradient Pb-acetate solutions, and the results showed that the average escape latency of mice was prolonged and the number of times they crossed the platform position was reduced, suggesting that Pb exposure significantly impaired the learning and memory functions of mice [29; 30]. In this study, the MWM test revealed that the mice in the Pb-exposed group swam chaotically and purposelessly and were unable to accurately locate the quadrant and position of the platform, and the average latency to escape was prolonged, which indicated that the mice's spatial localization and learning ability was impaired; the number of times the mice traversed the platform and the time of the first time they reached the platform were higher than those of the control group after the platform was withdrawn, which indicated that their memory was impaired by the Pb, which was in line with the results of the previous studies [28; 30]. Combined with the results  
Figure 7: Pb exposure promotes miR-671 expression to induce cleavage of CDR1 as by AGO2. (**A**) Expression levels of miR-671-5P in the hippocampus of mice in each group after 10 months of Pb exposure. The data shown are expressed as the mean \(\pm\) SD, \(\mathbf{{}^{**}}\)\(p<\) 0.01, \(n=4\). (**B,C**) Expression levels of AGO2 gene and protein in the hippocampus of mice in each group after 10 months of Pb exposure. The data shown are expressed as the mean \(\pm\) SD, \(\mathbf{{}^{*}}\)\(p<\) 0.05, \(\mathbf{{}^{**}}\)\(p<\) 0.01, \(n=4\).