The effect of vitamin D supplementation on the brain mapping and behavioral performance of children with ADHD: a double-blinded randomized controlled trials.

BACKGROUND: Attention deficit hyperactivity disorder (ADHD) is one of the common neurodevelopmental diseases that are accompanied with EEG pattern changes and Low levels of 25-hydroxyvitamin D [25(OH)D]. Neurofeedback provides a feedback signal to alleviate brain wave abnormalities and offers an alternative therapy for ADHD. This study aimed to investigate the concomitant effects of Vitamin D3 supplementation and Neurofeedback on children with ADHD. METHOD: This study was implemented on children with an established diagnosis of ADHD who received multisession Neurofeedback therapy. The intervention and control groups received 50000 IU vitamin D3 capsules and placebo respectively once a week for 2 months. The background rhythm was measured using quantitative EEG both before and at the end duration of the therapy. RESULTS: All of the vitamin D3 treated children showed a significant increase in the 25(OH)D (46 ± 18, 28 ± 10 (ng/ml), p = 0.001) and serum calcium level (9.5 ± 0.5, 9.8 ± 0.3 (mg/dl), p = 0.003) compared to the baseline. There were a statistically significant decrease in the treatment group about theta relative power, theta/beta, and theta/alpha power ratios within two eyes conditions (p = 0.004). All the changes were significant within eye open state in the treatment group (2.4 ± 1.2, 1.7 ± 0.5, p = 0.01). There is a significant relationship between Connors scores and some brain waves improvement (in relative theta (r = 0.998) and theta-to-beta power difference score (r = 0.56) (p < 0.001). CONCLUSION: Concomitant use of vitamin D3 supplementation and neurofeedback, increases the serum level of this vitamin and reveal favorable electrophysiological results in children with ADHD.Trial registration: Iranian Registry of Clinical Trials identifier: IRCT20200922048802N1..

Time estimation and beta segregation: An EEG study and graph theoretical approach.

Elucidation of the neural correlates of time perception constitutes an important research topic in cognitive neuroscience. The focus to date has been on durations in the millisecond to seconds range, but here we used electroencephalography (EEG) to examine brain functional connectivity during much longer durations (i.e., 15 min). For this purpose, we conducted an initial exploratory experiment followed by a confirmatory experiment. Our results showed that those participants who overestimated time exhibited lower activity of beta (18-30 Hz) at several electrode sites. Furthermore, graph theoretical analysis indicated significant differences in the beta range (15-30 Hz) between those that overestimated and underestimated time. Participants who underestimated time showed higher clustering coefficient compared to those that overestimated time. We discuss our results in terms of two aspects. FFT results, as a linear approach, are discussed within localized/dedicated models (i.e., scalar timing model). Second, non-localized properties of psychological interval timing (as emphasized by intrinsic models) are addressed and discussed based on results derived from graph theory. Results suggested that although beta amplitude in central regions (related to activity of BG-thalamocortical pathway as a dedicated module) is important in relation to timing mechanisms, the properties of functional activity of brain networks; such as the segregation of beta network, are also crucial for time perception. These results may suggest subjective time may be created by vector units instead of scalar ticks.

Gene expression study of mitochondrial complex I in schizophrenia and paranoid personality disorder.

OBJECTIVES: The aetiology and molecular mechanisms of schizophrenia (SCZ) and paranoid personality disorder (PPD) are not yet clarified. The present study aimed to assess the role of mitochondrial complex I and cell bioenergetic pathways in the aetiology and characteristics of SCZ and PPD. METHODS: mRNA levels of all genomic and mitochondrial genes which encode mitochondrial complex I subunits (44 genes) were assessed in blood in 634 SCZ, 340 PPD patients and 528 non-psychiatric subjects using quantitative real-time PCR, and associated comprehensive psychiatric, neurological and biochemical assessments. RESULTS: Significant expression changes of 18 genes in SCZ patients and 11 genes in PPD patients were detected in mitochondrial complex I. Most of these genes were novel candidate genes for SCZ and PPD. Several correlations between mRNA levels and severity of symptoms, drug response, deficits in attention, working memory, executive functions and brain activities were found. CONCLUSIONS: Deregulations of both core and supernumerary subunits of complex I are involved in the aetiology of SCZ and PPD. These deregulations have effects on brain activity as well as disorder characteristics.