Alleviating Learning & Concentration Impairments in Parkinson's Disease

Overview

Parkinson’s Disease (PD), a neurodegenerative disorder, is caused by the death of dopaminergic neurons in the substantia nigra. Caffeine exposure is suggested to mitigate the PD onset and progression by slowing the death of the dopaminergic neurons. Isolating the caffeine induced gene expression and the associated interaction pathways that target the dopaminergic death in the substantia nigra of a PD patient is vital for preventing or slowing the progression of the disease. Even though a number of genes have been identified to be related to PD, no direct correlation between the caffeine trigger and the associated pathways has been provided and explained. The Sodium Channel Subunit Beta-1 (SCN1B) gene and the novel voltage-gated sodium channel (VGSC) complex pathway triggered by it have not been adequately researched previously. This research study concludes that caffeine exposure at 93 mg/kg down-regulates the SCN1B gene, triggering a novel voltage-gated sodium channel complex pathway, blocking the sodium channel to negatively influence (reduce) cognitive impairment. This results in mitigating PD as a result of reduced neuronal damage in substantia nigra. GEO2R volcano plot analysis of microarray datasets identified that a caffeine trigger down-regulated differentially expressed gene, SCN1B. Results from String enriched network interactions suggested that SCN1B is identified to trigger 9 interactions (pathways) across different genes. Research conducted in vitro to determine the effect of various concentrations of caffeine on SHSY5Y cells with an overexpression of alpha-synuclein produced that high dosages ( >5 mM) may impose toxic effects, low dosage (<0.05 mM) did not produce a positive effect, but dosage of 0.5 mM (~93 mg/kg) was effective. This research unleashes the potential to administer a regimented caffeine dosage to both proactively prevent and reactively slow down the progression of the PD.