| pubmed-article:10510188 | pubmed:abstractText | In recent years, repetitive transcranial magnetic stimulation (rTMS) of the human brain has been used as a therapeutic tool in a variety of psychiatric and neurological disorders. However, to understand the mechanisms underlying any potential therapeutic effects, and possible adverse effects, studies are necessary on how magnetic stimuli induced by rTMS interact with central nervous system (CNS) regulation. In the current study, we failed to find cognitive impairments or structural alterations in rat brains after 11 weeks of long-term treatment with rTMS, which if present would indicate neuronal damage. In contrast, our in vitro studies showed that magnetic stimulation analogous to rTMS increased the overall viability of mouse monoclonal hippocampal HT22 cells and had a neuroprotective effect against oxidative stressors, e.g. amyloid beta (Abeta) and glutamate. The treatment increased the release of secreted amyloid precursor protein (sAPP) into the supernatant of HT22 cells and into cerebrospinal fluid from rats. HT22 cells preincubated with cerebrospinal fluid from rTMS-treated rats were found to be protected against Abeta. These findings suggest that neurochemical effects induced by rTMS do not lead to reduced neuronal viability, and may even reduce the detrimental effects of oxidative stress in neurons. | lld:pubmed |
