Multifactorial effects of short duration early exposure low intensity magnetic field stimulation in Streptozotocin induced Alzheimer's disease rat model.

Alzheimer's disease (AD) is an approaching, progressive public health crisis which presently lacks an effective treatment. Various non-invasive novel therapies like repetitive transcranial magnetic stimulation have shown potential to improve cognitive performance in AD patients. In the present study, the effect of extremely low intensity magnetic field (MF) stimulation on neurogenesis and cortical electrical activity was explored. Adult Wistar rats were divided into Sham, AD and AD + MF groups. Streptozotocin (STZ) was injected intracerebroventricularly, at a dose of 3 mg/kg body weight for developing AD model. The AD rats were then exposed to MF (17.96 µT) from 8th day of STZ treatment until 15th day, followed by cognitive assessments and electrocortical recording. In brain tissue samples, cresyl violet staining and BrdU immunohistochemistry were done. MF exposure, improved passive avoidance and recognition memory, attenuated neuronal degeneration and enhanced cell proliferation (BrdU positive cells) in comparison to AD rats. It also significantly restores delta wave power from frontal lobe. Our results suggest that early-stage MF exposure could be an asset for AD research and open new avenues in slowing down the progression of Alzheimer's disease.

Cytomorphological Analysis and Interpretation of Nitric Oxide-Mediated Neurotoxicity in Sleep-Deprived Mice Model.

Background: Sleep deprivation (SD) is a biological stress condition for the brain, and the pathogenesis of SD is closely related to elevated oxidative stress, mitochondrial dysfunction, a major cause of neurodegeneration. This oxidative stress-mediated cell death is attributed to rise in calcium ion influx which further excites or alters the neurotransmitters level by activating neuronal nitric oxide (NO) synthase (nNOS) release of NO in mouse SD model. This study indicates that the nitrergic neurons are possible therapeutic targets for the amelioration of SD-induced cognitive dysfunction and behavioral alterations. Purpose: SD is considered as a risk factor for various neurodegenerative diseases. SD leads to biochemical, behavioral, and neurochemical alterations in animals. This study was designed to explore the possible involvement of a nitrergic neuron system in six days SD-induced morphological and neurodegenerative changes in mice. Methods: Using nNOS immunohistochemistry, we have investigated the effects of SD on nNOS positive neurons. Immunohistochemical study for the distribution of nNOS positive neuronal cell bodies was carried out in the hippocampus, prefrontal cortex (PFC), and amygdaloid nuclei of mice brain. Results: Sleep-deprived animals showed a significantly increased number of nNOS positive neurons and altered neuronal cytomorphology as compared with the control group. Conclusion: These results indicate that total SD may induce morphological changes in nNOS positive neurons in the brain, thus increasing NO synthesis, which is implicated in SD-induced neuronal cell death.