Elevated Gaussian-modeled beta power in the cortex characterizes aging, but not Parkinson's disease.

Aging is a key risk factor for the development of Parkinson's disease (PD). PD is characterized by excessive synchrony of beta oscillations (13-30 Hz) in the basal ganglia thalamo-cortical network. However, cortical beta power is not reliably elevated in individuals with PD. Here, we sought to disentangle how resting cortical beta power compares in younger controls, older controls, and individuals with PD using scalp electroencephalogram (EEG) and a novel approach for quantifying beta power. Specifically, we used a Gaussian model to determine if sensorimotor beta power distinguishes these groups. In addition, we looked at the distribution of beta power across the entire cortex. Our findings showed that Gaussian-modeled beta power does not differentiate individuals with PD (on medication) from healthy younger or older controls in sensorimotor cortex. However, beta power (and not theta or alpha) was higher in healthy older versus younger controls. This effect was most pronounced in regions near sensorimotor cortex including the frontal and parietal areas [P < 0.05, false discovery rate (FDR) corrected]. In addition, the bandwidth of the periodic beta was also higher in healthy older than young individuals in parietal regions. Finally, the aperiodic component, specifically the exponent of the signal, was higher (steeper) in younger controls than in individuals with PD in the right parietal-occipital region (P < 0.05, FDR corrected), possibly reflecting differences in neuronal spiking. Our findings suggest that cortical Gaussian beta power is possibly modulated by age and could be further explored in longitudinal studies to determine whether sensorimotor beta increases with increasing age.NEW & NOTEWORTHY Altered sensorimotor beta activity has been shown to be a feature in aging and PD. Using a novel approach, we clarify that resting sensorimotor beta power does not distinguish subjects with PD from healthy younger and older controls. However, beta power was higher in older compared with younger controls in central sensorimotor, frontal, and parietal regions. These results provide a clearer picture of sensorimotor beta power, demonstrating that it is elevated in aging but not PD.

Novel approaches for quantifying beta synchrony in Parkinson's disease.

Despite the clinical and financial burden of Parkinson's disease (PD), there is no standardized, reliable biomarker to diagnose and track PD progression. Instead, PD is primarily assessed using subjective clinical rating scales and patient self-report. Such approaches can be imprecise, hindering diagnosis and disease monitoring. An objective biomarker would be beneficial for clinical care, refining diagnosis, and treatment. Due to widespread electrophysiological abnormalities both within and between brain structures in PD, development of electrophysiologic biomarkers may be feasible. Basal ganglia recordings acquired with neurosurgical approaches have revealed elevated power in the beta frequency range (13-30 Hz) in PD, suggesting that beta power could be a putative PD biomarker. However, there are limitations to the use of beta power as a biomarker. Recent advances in analytic approaches have led to novel methods to quantify oscillatory synchrony in the beta frequency range. Here we describe some of these novel approaches in the context of PD and explore how they may serve as electrophysiological biomarkers. These novel signatures include (1) interactions between beta phase and broadband (> 50 Hz, "gamma") amplitude (i.e., phase amplitude coupling, PAC), (2) asymmetries in waveform shape, (3) beta coherence, and (4) beta "bursts." Development of a robust, reliable, and readily accessible electrophysiologic biomarker would represent a major step towards more precise and personalized care in PD.