Assessing the Neurobiological Modulation Results of Radioeletric asymmetric conveyer (REAC) on Salivary Metabolomics in Parkinson's Disease.

Parkinson's disease (PD) is a multifaceted neurodegenerative disease characterized by motor and non-motor symptoms resulting from the degeneration of dopaminergic neurons in the brain. Endogenous Bioelectrical Activity (EBA) plays a crucial role in cellular physiology, intercellular communication and tissue organization, making it a focal point for neurobiological modulation therapies such as REAC technology. This raises the question of whether REAC protocols, specifically neuropostural optimization (NPO) and neuropsychophysical optimization (NPPO), can induce EBA changes measurable in saliva metabolomics in PD patients. Purpose: This study seeks to evaluate salivary metabolic profiles in individuals with PD undergoing NPO and NPPO with REAC technology. Methods: Salivary samples from 33 patients were collected and analyzed using Nuclear Magnetic Resonance (NMR) spectroscopy on a 500 MHz Bruker Biospin device (Rheinstetten, Germany). The resulting NMR spectra were then subjected to Principal Component Analysis (PCA) to identify patterns in the data. Additionally, discriminant analyses were performed using the Partial Least Squares (PLS-DA) and Sparse Partial Least Squares (sPLS-DA) methods to differentiate between pre- and post-therapy metabolomic profiles. The quality of the predictive models was evaluated using the Q2 metric (prediction quality), R2 metric (quality of adjustments), and accuracy (ACC). Univariate analyses were also conducted, adopting a 95% confidence interval to determine the significance of changes in metabolite levels. Results Significant changes in the metabolomic profile were observed after the NPO and NPPO-REAC cycles, affecting a panel of 27 metabolites. Multivariate analysis revealed variations in metabolite abundances before and after the therapy. Specifically, decreases were noted in acetic acid, isocaproate, saturated fatty acids, ketovaleric acid, hydroxyproline, isoleucine, butyric acid, N-caproate, lysine, lipids, and histidine. Conversely, increases were observed in sarcosine, threonine, valine, lactate, sucrose, leucine, and propionic acid, along with other unmarked metabolites. These changes suggest that REAC therapy can significantly alter the metabolomic profile. Conclusion: significant changes in the salivary metabolic profile highlight biochemical changes associated with the intervention, indicating systemic effects that deserve further investigation. These findings collectively suggest promising therapeutic effects and argue for the continued exploration and use of REAC technology in the treatment of neurodegenerative diseases.