Molecular mechanisms of transcranial electrical stimulation that help reduce protein accumulation underlying neurodegenerative diseases have been revealed by the “Direct current stimulation enhances neuronal alpha-synuclein degradation in vitro”, study, recently published on Scientific Reports, created by Gessica Sala, a technologist at NeuroMi – Milan Center for Neuroscience, directed by Carlo Ferrarese.
Through a human neuronal model, the study demonstrated that direct current stimulation (DCS) can interfere with the aggregation and degradation of alpha-synuclein protein, the accumulation of which is associated with neuronal degeneration in Parkinson’s disease patients.
In addition to researchers from Milano-Bicocca, the study involved the collaboration of neurologists Tommaso Bocci and Alberto Priori, both from the Department of Human Sciences – “Aldo Ravelli” Centre for Neurotechnology and Experimental Neurological Therapies, Department of Health Sciences (University of Milan and ASST Santi Paolo e Carlo, Milan) experts in neurostimulation techniques applied to different neurological conditions including Parkinson’s disease, and Marta Parazzini, an engineer at the Institute of Electronics and Information and Telecommunications Engineering (CNR, Milan).
Transcranial direct-current stimulation (tDCS) has been used for years as a non-invasive and safe technique to modulate neuronal excitability in patients suffering from various diseases including stroke, psychiatric diseases and movement disorders, including Parkinson’s disease. In particular, in patients with Parkinson’s disease tDCS is proposed as a valid therapeutic option, in addition to pharmacological treatment, since it is proven to be clinically effective in improving motor and non-motor symptoms typical of the disease.
Although there is plenty of literature data on the clinical benefits of tDCS, its action mechanisms remain largely unclear. Moreover, to date this technique is used as a symptomatic treatment and its neuroprotective potential, i.e. its ability to modify and slow down the course of the disease, remains completely unexplored.
This research has made it possible to devise a useful experimental model for the in vitro study of the biological effects of DC stimulation and, above all, to show that the clinical effects of tDCS observed in patients can directly counteract the main pathogenetic mechanism of Parkinson’s disease, namely the aggregation and subsequent intracellular accumulation of alpha-synuclein.
“The findings from this study,” said Gessica Sala, the first author of the research, “lay the groundwork for further identification of intracellular mechanisms associated with tDCS, in relation not only to its effect on alpha-synuclein, but also on other aggregation-prone proteins involved in the pathogenesis of other important neurodegenerative diseases by protein accumulation, such as Alzheimer’s disease and amyotrophic lateral sclerosis (ALS).”
“Further understanding of these findings will help to identify and select patients with Parkinson’s disease,” added Tommaso Bocci, “and possibly other neurodegenerative diseases that may benefit from the treatment.”