DEPRESSION in Parkinson’s disease (PD) was linked to distinctive patterns of brain activity within the pallidum, according to new research that identified a potential biomarker for neuropsychiatric symptoms in this complex neurodegenerative disorder.
Depression affects up to half of patients with PD and represents a major contributor to disability and reduced quality of life. Despite its high prevalence, the neurobiological mechanisms underlying depression in PD have remained poorly understood, limiting the development of targeted therapeutic strategies. Previous studies have associated depressive symptoms with abnormal neural activity in the subthalamic nucleus, but the role of other basal ganglia structures has been less well defined.
Pallidal Beta Power Identifies Depression in Parkinson’s Disease
In this retrospective study, investigators examined whether pallidal beta power was associated with depression symptoms in patients with PD undergoing deep-brain stimulation (DBS) implantation surgery. The analysis included 50 patients who underwent intraoperative recordings of resting-state neural activity from the pallidum during DBS surgery.
Patients with clinically elevated depression symptoms exhibited significantly higher beta-frequency oscillations, defined as 13–30 Hz, compared with patients without depression. Pallidal beta power was also associated with depression severity, even after adjusting for demographic characteristics, PD-related clinical variables, medication use, and other neurophysiological factors.
These findings expanded existing evidence linking basal ganglia circuitry to psychiatric symptoms in PD and positioned the pallidum as a key structure alongside the subthalamic nucleus.
Implications for DBS and Personalised Care
PD is a progressive neurodegenerative disorder characterised by motor symptoms such as tremor, rigidity, and bradykinesia, alongside non-motor features including depression, anxiety, and cognitive impairment. DBS is an established therapy for motor complications in PD, but its effects on psychiatric symptoms have been inconsistent and difficult to predict.
The identification of pallidal beta power as a potential biomarker raised the possibility of tailoring DBS parameters to better address depressive symptoms. Targeting pathological beta activity may allow clinicians to optimise neuromodulation strategies for both motor and non-motor outcomes in PD.
The study was limited by its modest sample size and reliance on intraoperative recordings that captured neural activity at a single time point. Future studies with longitudinal monitoring should explore whether direct modulation of pallidal beta power can improve depression outcomes in PD. DBS is also increasingly being investigated for treatment-resistant depression in the general population, highlighting the growing role of circuit-based therapies in psychiatry.
Overall, these findings provided new insight into the neurobiology of depression in PD and supported future efforts to personalise DBS therapy for psychiatric symptoms.
Reference
Johnson KA et al. Pallidal beta power is associated with depression in Parkinson’s disease. npj Parkinsons Dis. 2026; DOI:10.1038/s41531-026-01264-4.
