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. 2019 Mar 30;7(2):19. doi: 10.3390/toxics7020019

Figure 9.

Figure 9

Proposed cognition-enhancing mechanism of CA in D-gal and AlCl3 induced rats. Administration of D-gal/AlCl3 induced oxidative stress, cholinergic dysfunction and apoptosis. Administration of CA decreased the levels of AChE and MDA by blocking their activities. CA also increased the levels of SOD and maintain the neuronal cytoarchitecture by prevention of apoptosis.