Extremely low intensity magnetic field effectively improves cognitive impairment in intracerebroventricular streptozotocin animal model sparing septo‐hippocampal cholinergic pathway and CAMKII

Abstract

We have investigated the role of extremely-low-frequency magnetic field (ELF-MF, 17.96µT, 50Hz, 2hr/day for 60 days) exposure on i.c.v. streptozotocin (STZ, 3mg/kg bw, bilaterally, single bolus) induced rat model of AD in a customized chamber. Spatial memory and recognition memory was measured using Morris water maze and one trial object recognition task respectively. Further, acetylcholine, acetylchoniesterase, calcium-calmodulin dependent protein kinase II from frontal cortex and hippocampus and serum Aß1-42 was measured using colorimetric or ELISA technique. Spatial memory in Morris water maze (MWM) showed a significant decrease both in the distance travelled before entering into goal quadrant (p=0.05) as well as in latency to the first entry into goal quadrant (p=0.05) in AD animals, upon ELF-MF exposure. On the other hand, recognition index (p=0.003) and discrimination index (p<0.0001) in the one trial object recognition test (OTORT) on the 60th day after ELF-MF exposure to STZ animals showed a significant increment when compared with AD induced animals. These behavioural results suggests an improvement in cognitive function in i.c.v. STZ animals, upon exposure to ELF-MF. When we looked for serum Aß1-42 of experimental animals, we found a significant reduction (p=0.05) of serum Aß1-42 in AD animals after ELF-MF exposure. Further, concentration of acetylcholine (ACh) was found to be increased (p=0.05) only in hippocampus, whereas AChE level was found to be reduced in both frontal cortex (p=0.05) as well as in hippocampus (p=0.05) after 60 day ELF-MF treatment in i.c.v. STZ animals. Expression of CAMKII increased in frontal cortex (p=0.05) as well as in hippocampus (p0.05) after ELF-MF treatment. These results suggests that memory retention observed in the behavioural results, may be due to the reduction of AChE in hippocampus as well as in frontal cortex, Aß1-42 in serum, and an increase in levels of ACh, CAMKII in hippocampus as well as in the frontal cortex. Therefore, evidences strengthens the notion that, ELF-MF treatment improves cognitive impairment seen in i.c.v. STZ animal model of AD through prevention of synaptic dysfunction, replenishment of ACh as well as CAMKII in hippocampus.