What Causes Midbrain Activation?

Neuronal degenerative diseases such as Parkinson's disease and Alzheimer's disease are closely related to physically-gated ion channels, which can be solved by physical means. Activation of neurotransmitters is the key to treatment, while voltage-gated calcium channels Is the best target for physical activation, the purpose is to induce calcium influx to trigger neuronal axon terminal synaptic vesicles to release neurotransmitters. ^[1]

Brain cell activation theory

(Scientific theory)

A technique based on transcranial magnetoelectric stimulation ^[2]

Core theory of brain cell activation theory: Parkinson's disease (PD), Alzheimer's disease (AD) and other neurodegenerative diseases, which are closely related to physically gated ion channels, can be solved by physical means to activate transmitter energy Neurons are the key to treatment, and voltage-gated calcium channels are the best targets for physical activation. The purpose is to induce calcium influx to trigger neuronal axon terminal synaptic vesicles to release neurotransmitters. ^[1]

Animal experiments were used to detect the positive correlation between Transcranial Magnetoelectric Stimulation Technology (TME) and the amount of dopamine and acetylcholine produced in the brain, and clinical trials to observe the improvement of symptoms of PD and AD patients by TME.

Brain cell activation theory animal test

Parkinson's disease is closely related to the reduction of dopamine in the brain. This result has been repeatedly confirmed for half a century, and a large number of experiments have indirectly proved that TME has a positive correlation with endogenous dopamine production. The effect of transcranial magnetic stimulation on dopamine release in hippocampus, nucleus accumbens and striatum of adult male Wistar rats was detected by intracerebral microdialysis technology. It was found that transcranial magnetic stimulation can significantly increase dopamine concentrations in dorsal hippocampus, nucleus accumbens and striatum high. Transcranial magnetic stimulation activated dopaminergic neurons in PD model rats and promoted the release of endogenous dopamine in the ventral striatum. Adult hemiparkinsonian macaques with successfully installed stimulation electrodes were selected. As a result, electrical stimulation can effectively improve the symptoms of the PD model of the monkeys. Microdialysis sampling technology combined with high-performance liquid chromatography was used to find that after effective electrical stimulation was given It can increase the content of dopamine and its metabolites in extracellular fluid of lateral striatum. Studies have found that thalamic subnuclear electrical stimulation can increase dopamine release from rat striatum cells and activate dopaminergic neurons. It has been demonstrated that electrical stimulation can promote the release of endogenous opioid peptides in the center. Because neurotransmitters and neuropeptides coexist in neurons, it can be concluded that electrical stimulation also promotes the release of neurotransmitters. The effect of TME is much better than that of transcranial magnetism or transcranial electricity.

Clinical validation of brain cell activation theory

Since 1994, the idea that "activating brain cells is the key to treating various difficult encephalopathy" has been proposed. In the past two decades, the author has repeatedly verified and improved the theory of "brain cell activation" from theory to practice to theory. One explanation of its mechanism of action is that peptide peptide neurons, dopaminergic neurons, serotonergic neurons, and cholinergic neurons are mainly activated correspondingly. Among them, the authors applied non-invasive TME to the clinical application of Parkinson's disease, and conducted a multi-center, randomized, double-blind, self-cross-control method to conduct clinical trials on PD patients who met the inclusion criteria. The author also applied non-invasive TME to the treatment of Alzheimer's disease and vascular dementia. A multi-center, randomized, double-blind, placebo parallel control method was used to conduct clinical trials on AD patients who met the inclusion criteria. . ^[1]