In a previous study on the mechanism of JDYZF, we found that the extract of Coptis chinensis polysaccharide, the main drug component of JDYZF, improved the lifespan of the transgenic Caenorhabditis elegans CL4176 model of AD, reduced the paralytic rate, inhibited nematode head Aβ deposition, increased heat shock protein hsp16.2 and hsp16.41 gene expression levels [15], reduced the Aβ25–35-induced expression of cleaved-caspase-3 and Bax in PC12 cells, increased the expression of Bcl-2 and inhibited apoptosis [16]. Here, CASP3 is linked to Alzheimer disease.