Additionally, hippocampal CNTN1 overexpression appeared to cause cognitive deficits in mice, which coincided with the activation of microglia and astrocytes, leading to abnormal EAAT1/ EAAT2 expression with the blockade of synaptic LTP in the hippocampus, which could be prevented by minocycline. This evidence concerns the gene SLC1A3 and Cognitive impairment.