What is GammaPark?

Over the years, two EEG biomarkers have been identified in patients suffering from PD. The main oscillatory activity identified in the cortico-basal ganglia loop is a frequency band around 30 Hz, a pathological activity correlated with symptoms such as hypokinesia and rigidity [5, 6]. Treatments with dopaminergic drugs and deep brain stimulation can reduce this pathological oscillation and are associated with an improvement in symptoms [5]. However, After an initial “honeymoon” period when the standard dopamine replacement drug L-DOPA almost completely reversed the signs and symptoms of PD, the treatment starts losing its effectiveness [6] and induces motor complications, also called L-DOPA-induced Dyskinesia (LID).

Excessive cortical EEG Gamma oscillations have also clearly been identified in patients with PD during chronic dopaminergic treatment. This resonant oscillatory activity has been correlated with abnormal involuntary movements (LID) [8].

In animal models of PD, and more specifically in the unilateral 6-OHDA-lesioned rat, similar pathological EEG oscillations have been identified [9]. In these freely-moving animals, a strong cortical beta activity has indeed been characterized. Importantly, injection of dopaminergic drugs in these animals significantly reduced this cortical beta band (BetaPark), in association with contralateral rotations [8].

Halje et al. [10] also identified resonant cortical oscillations in the Gamma frequency range after chronic treatment with L-DOPA, which aligns with the clinical literature. These Gamma oscillations were found to be minimally affected by voluntary movements while their presence proved to be a reliable biomarker of L-DOPA-induced Dyskinesia.

In particular, excessive cortical EEG Gamma oscillations induced by chronic L-DOPA treatment in the 6-OHDA rat model can be viewed as a proxy for the cortico-basal ganglia loop dysfunction mentionned above which underlies LID.