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Product News

New Biomarker of Parkinson’s Disease Progression

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Product News

New Biomarker of Parkinson’s Disease Progression

SynapCell and Motac Neuroscience have discovered a new biomarker for monitoring the progression of Parkinson’s disease (PD). The BetaPark [evo] could enable opportunities for drug developers to test the neuroprotective or disease-modifying effects of their compounds. This discovery, combining Motac’s disease modeling and SynapCell’s EEG phenotyping capabilities, was presented in a poster in the Circuit Mechanisms of Motor Dysfunction in Parkinson's Disease Session of the Society for Neuroscience Annual Meeting in Chicago.

BetaPark [evo] will be commercially available to the pharmaceutical industry for PD preclinical drug discovery by Q2 2020.

“Neuronal degeneration begins years before clinical symptoms of Parkinson’s appear. And until now there have been no reliable animal models with relevant biomarkers to track disease progression and screen novel therapies,” says Yann Roche, Ph.D., Chief Innovation Officer at SynapCell. “With BetaPark [evo], we are proud to announce the identification of the first EEG biosignature to address the evolution of Parkinson’s disease and support pharmaceutical companies in developing neuroprotective strategies using objective, accurate and longitudinal metrics over time.”

SynapCell’s Cue® EEG methodologies have successfully highlighted aberrant Beta oscillations (BetaPark) as an in vivo biomarker to assess pharmacodynamics of anti-PD and anti-dyskinetic drug candidates in symptomatic rat models of PD since 2013. The goal of the two-year partnership between the two companies was to phenotype Motac’s Alpha-Synuclein rat model of PD progression using SynapCell’s Cue® EEG technology.

Research conducted through this partnership demonstrated the progressive rise of aberrant Beta synchronization over 12 weeks, alongside with disease progression in the clinically-relevant Alpha-Synuclein rat model. A correlation between neuron loss in the substantia nigra and the increase of BetaPark power was found. Moreover, when treated with L-DOPA, animals revealed a statistically significant decrease of BetaPark power, confirming that the biomarker is pharmacosensitive to this standard-of-care.

BetaPark [evo] could represent a clinically meaningful endpoint for the validation of neuroprotective experimental therapeutics, calling for clinical validation of this surrogate biomarker for neurodegenerative disorders.

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