Abstract
Intracerebroventricular streptozotocin injection at 3mg/kg of b/w causes phenotypes similar to that of sporadic Alzheimer’s disease (sAD) from 14th day post-injection. On the other hand, body of evidences indicated that impairment in the sAD is the major contributor for cognitive decline. Taken together, we tested the adult neurogenesis hypothesis in streptozotocin model of sAD in female Wistar rats after extremely low magnetic stimulation (MF: 17.96, 50Hz, 2hr/day, 21days). To do so, 33 rats were randomly divided into three groups viz. Sham+MF, AD and AD+MF. Consequently, animals were first induced AD with stereotaxic manipulation and then they were exposed to low frequency magnetic field stimulation and followed by terminal cognitive behavioral tasks brain tissue were isolated for both biochemical and subcellular expression experiments (ethical no. 12/IAEC-1/2017). Results showed reduction in latency to the goal quadrant (p= 0.002) and transfer latency (p= 0.045) in AD+MF group versus AD. Even, Dirichlet distribution of time spent in 4 quadrants indicated un-uniform in all the groups except AD group (p= 0.067, LRS= 7.35). Further, cell count in CA3 and DG exhibited increase in cell density in AD+MF group (p<.05). however, we found significant reduction in sod1 activity after mf treatment (p="0.035)" but no change gsh level hippocampus and frontal cortex. interestingly, these changes ad+mf animals are associated with increase density of brdu+ />Nestin+ cells in granular layer (p= 0.002) and hilus region (p= 0.0005) of DG along with increase in expression of L-type Ca2+ channels as compared to AD group. These experimental evidences suggests that noninvasive brain stimulation can promote adult neurogenesis by activating L-type ca2+ channels in the hilus, which intern helps in retention of long term memory even after sAD.