Dexmedetomidine mediates the mechanism of action of ferroptosis in mice with Alzheimer’s disease by regulating the mTOR-TFR1 pathway

Table 1 Comparison of escape latency, number of platform crossings and target quadrant residence time in the different treatment groups

Groups	Sham (n = 10)	Aβ (n = 10)	Dex (n = 10)	Dex + rapamycin (n = 10)
Escape latency (s)	5.38 ± 0.53	42.20 ± 3.89a	13.81 ± 1.64a,b	22.75 ± 3.06a,b,c
Number of platform crossings (times)	7.26 ± 0.82	1.38 ± 0.35a	5.90 ± 0.61a,b	3.24 ± 0.43a,b,c
Target quadrant residence time (s)	38.46 ± 5.27	7.92 ± 1.69a	30.40 ± 4.26a,b	22.52 ± 2.78a,b,c

^aP < 0.05, compared with the sham group.

^bP < 0.05, compared with the amyloid β group.

^cP < 0.05, compared with the dexmedetomidine group.

β: Amyloid β; Dex: Dexmedetomidine.