Transcranial magnetic stimulation in animal models of neurodegeneration

Abstract

Brain stimulation techniques offer powerful means of modulating the physiology of specific neural structures. In recent years, non-invasive brain stimulation techniques, such as transcranial magnetic stimulation (TMS) and transcranial direct current stimulation, have emerged as therapeutic tools for neurology and neuroscience. However, the possible repercussions of these techniques remain unclear, and there are few reports on the incisive recovery mechanisms through brain stimulation. Although several studies have recommended the use of non-invasive brain stimulation in clinical neuroscience, with a special emphasis on TMS, the suggested mechanisms of action have not been confirmed directly at the neural level. Insights into the neural mechanisms of non-invasive brain stimulation would unveil the strategies necessary to enhance the safety and efficacy of this progressive approach. Therefore, animal studies investigating the mechanisms of TMS-induced recovery at the neural level are crucial for the elaboration of non-invasive brain stimulation. Translational research done using animal models has several advantages and is able to investigate knowledge gaps by directly targeting neuronal levels. In this review, we have discussed the role of TMS in different animal models, the impact of animal studies on various disease states, and the findings regarding brain function of animal models after TMS in pharmacology research.

Keywords: Alzheimer’s disease; Parkinson’s disease; depression; glial cells; neurorehabilitation; repetitive transcranial magnetic stimulation; transcranial direct current stimulation; transcranial magnetic stimulation.

Figure 1

The beneficial effects of TMS on neuronal recovery. TMS treatment inhibits neuronal cell death by regulating various cell signaling pathways and significantly improves neural functioning due to its protective and therapeutic effects as cellular levels. AKT: Protein kinase B; Bcl-2: B-cell lymphoma 2; Bcl-xL: B-cell lymphoma-extra large; BDNF: brain-derived neurotrophic factor; CREB: cyclic AMP response-element binding protein; ERK: extracellular signal-regulated kinase; GABA: gamma-aminobutyric acid; NMDA: N-methyl-D-aspartate; TMS: transcranial magnetic stimulation; TrkB: tropomysin related kinase B.