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

Background: 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. Method: 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. Result: 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. Conclusion: 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. [ABSTRACT FROM AUTHOR]