Investigation of EEG changes during exposure to extremely low-frequency magnetic field to conduct brain signals.

There are evidences that confirm the effect of magnetic fields (MFs) on brain signals and some psychological disorders such as headache, migraine and depression. The aim of the present study was to investigate changes in EEG power spectrum due to localized exposure in different parts of the brain by extremely low-frequency magnetic fields (ELF-MFs) to extract some protocols for treatment of some psychological disorders. In addition, regular effects were investigated by increasing intensity of ELF-MF. Therefore, EEG relative power spectrum was evaluated at T4, T3, F3, F4, and Cz points, when all the points were exposed to MFs with 45, 17, 10, 5, and 3 Hz frequencies, separately. Intensity of MF was 0, 100, 240, or 360 µT in four sessions. Significant changes were observed in different EEG bands caused by locally exposing to ELF-MF in different points of brain (P < 0.05). Some exposure to MFs decreased alpha band of frontal and central areas in closed-eyes state. Based on the findings in this study, some protocols can be designed using a combination of various MFs exposures to conduct the brain signals that is necessary to evaluate clinically.

Mitochondrial and nuclear genes as the cause of complex I deficiency.

Multiple sclerosis (MS) is an immunological inflammatory disease of the central nervous system. The pathogenesis of MS is incompletely understood, but various studies have suggested that mitochondrial dysfunction is associated with the disease. Mitochondria are among the main cellular sources of reactive oxygen and nitrogen species, and they play a pivotal role in many neuro-pathological conditions. The mitochondrial nuclear subunit of complex I gene in mitochondria may play a role in MS, and understanding this role may provide rationale for novel approaches to treatment of the disease and the development of novel therapies. We designed a molecular study to demonstrate biochemical defects in complex I activity and found some novel nucleotide substitutions in mitochondrial DNA that might be involved in the pathogenesis of MS. The mitochondrial complex subunit I sequence was amplified and sequenced in MS patients. Although no reported pathogenic mutations were found in these patients, other studies have clearly indicated that the mitochondrial nuclear complex subunit I gene plays a significant role in MS pathogenesis.

Study of the frequency parameters of EEG influenced by zone-dependent local ELF-MF exposure on the human head.

It has been reported that human subjects exposed to electromagnetic fields exhibit changes in human EEG signals at the frequency of stimulation. The aim of the present study was to expose different parts of the brain to extremely low-frequency magnetic fields locally and investigate EEG power spectrum alters at the frequency of stimulation. EEG relative power spectrum were evaluated at 3, 5, 10, 17, and 45 Hz frequencies at T4, T3, F3, Cz, and F4 points, respectively, when these points were exposed to magnetic fields with similar frequencies and 100 µT intensity. The paired t-test results showed that power value of EEG did not alter significantly at the frequency of stimulation (P<0.05). Further, significant changes in different EEG bands caused by locally exposing to ELF-MF in different points of brain were observed. The changes in the EEG bands were not limited necessarily to the exposure point.

Skew in the human caveolin 1 gene upstream purine complex homozygote haplotype compartment in multiple sclerosis.

Caveolin 1 (CAV1) is a component of the myelin sheath and the expression of the gene encoding this protein is increased during myelination in Schwann cells and oligodendrocytes. We sought to investigate the homozygote haplotype compartment in a recently identified polymorphic purine complex at the upstream region of the human CAV1 gene in multiple sclerosis (MS). In a case/control study design, the region was characterized in 126 cases of MS diagnosed based on the Revised McDonald diagnostic criteria, and 460 controls. We report a skew in the homozygote haplotype compartment in the cases versus controls both in a qualitative and quantitative respect. Excess homozygosity for haplotypes was observed in the MS cases (corrected p<0.012, OR=2.54, CI 1.14-5.64). Furthermore, we observed eight homozygote haplotypes in the MS cases that were non-existent in the controls (p<0.0003, OR=20.27, CI 2.50-163.8). For the first time, our data highlight the CAV1 upstream purine complex as a novel susceptibility genomic locus in the pathophysiology of MS. Of utmost importance, the region has been conserved across species, including mouse, guinea pig, rhesus macaque, and human. The functional effect of this region remains to be clarified in the future studies.