MUMBAI: ‘Parkinson’s disease‘ (PD) is a degenerative condition affecting primarily the central nervous system. Statistics from 2020 indicate that over 10 million individuals globally were affected by Parkinson’s disease, with India accounting for 10% of cases. PD patients exhibit symptoms including trembling extremities, rigid muscles, and bradykinesia. Beyond these observable motor symptoms, patients experience non-motor manifestations, including anhedonia and reduced motivation, linked to dopamine deficiency. Dopamine, recognised as the ‘feel-good’ hormone, is naturally released during pleasurable activities or reward reception.The capacity to experience pleasure and rewards is crucial for human wellbeing. Dopamine generates pleasant sensations, encouraging individuals to pursue similar experiences or repeat rewarding actions. In PD patients, dopamine deficiency results in unusual brain activity and compromised reward processing, affecting their ability to identify, evaluate and react to rewarding stimuli.Scientists from the Human Motor Neurophysiology and Neuromodulation Lab at IIT Bombay’s Department of Biosciences and Bioengineering conducted research using brain signals to examine reward processing in PD patients.“In PD, motor symptoms like stiffness and tremors are typically the first noticeable signs, while the non-motor symptoms, including cognitive and emotional changes, often emerge years earlier. Some patients experience cognitive or emotional changes early on, while others may develop them much later, making it difficult to establish a consistent sequence of symptom onset,” remarks Prof. Nivethida, who led the study.Neurons communicate via electrical signals. Electroencephalography (EEG) records brain electrical activity using scalp-mounted metal discs. When performing tasks, EEG detects variations in electrical patterns within relevant brain regions. The research analysed EEG data from 28 PD patients and 28 healthy participants during reward-based learning tasks. PD patients’ EEG recordings were taken before (OFF condition – 15 hours post-medication) and after dopamine medication (ON condition), enabling assessment of medication effects on reward processing.The researchers employed three analytical methods to understand reward-related brain activity. The Event-related Potential (ERP) analysis revealed that 250-500 milliseconds post-reward, frontal brain regions typically show reward positivity. This positive EEG waveform response is vital for attention, learning, and emotional processes.Time-frequency analysis identified theta waves (5-7 Hz) and gamma waves (30-55 Hz), corresponding to different cognitive states. Theta waves correlate with reward processing and creativity, whilst gamma waves relate to decision-making and problem-solving. Phase-amplitude coupling (PAC) measured theta-gamma wave synchronisation, which facilitates inter-regional brain communication. This synchronisation is essential for reward processing and goal-directed behaviour.The findings demonstrated reduced reward positivity in PD patients’ ERPs, indicating ineffective reward processing. Dopamine medication failed to normalise this response. “Normally, the brain releases dopamine as short bursts following a reward, but in PD, these bursts are weaker. Although dopamine medication replenishes the dopamine levels in the brain, it does not produce burst-like signals that mimic the natural process.This could be the reason why dopamine is able to improve motor symptoms but not cognitive functions like reward processing. Hence, adjunct treatment strategies may be required to restore cognitive impairments in PD,” adds Prof. Nivethida.Time-frequency analysis showed diminished reward-related wave activity in PD patients during both ON and OFF conditions, compared to healthy individuals, suggesting persistent reward insensitivity despite medication. “These results also suggest that reward processing mediated by theta activity may not be driven purely by dopaminergic mechanisms and that the role of other chemicals in the brain (neurotransmitters) should not be ignored,” says Prof.Nivethida.PAC analysis revealed reduced theta-gamma synchronisation in PD patients, indicating impaired communication between reward-processing brain regions. This potentially explains their reduced motivation and compromised decision-making. Dopamine medication partially improved theta-gamma synchronisation, suggesting its potential as a biomarker for reward mechanism impairment in PD.“Reward processing deficits are not only reported in PD. They are also observed in other neuropsychiatric conditions such as depression, schizophrenia, and other movement disorders. This overlap complicates its use as a specific early biomarker for PD without additional supporting evidence,” suggests Prof. Nivethida.The research noted elevated posterior gamma activity in patients compared to healthy individuals, with longer disease duration correlating with increased gamma activity. This suggests the gamma pattern relates to disease progression rather than reward processing. The study emphasises how disrupted brain activity patterns affect specific cognitive functions in PD patients.The IIT Bombay research establishes links between abnormal brain activity and impaired reward appreciation in PD patients, whilst exploring reward processing mechanisms. It provides understanding of PD’s neural mechanisms and emphasises the necessity for supplementary treatments, such as non-invasive brain stimulation, for non-motor symptom improvement. The study underscores how proper reward processing and motivation maintenance contribute to life quality.