New Study Reveals How Brain Changes Impact Thinking Among Parkinson’s Patients

Bombay: A new study by researchers at the Indian Institute of Technology (IIT) Bombay has provided key insights into how disrupted brain activity affects cognitive function in people with Parkinson’s. The research highlights how impaired reward processing in the brain may explain common non-motor symptoms such as lack of motivation and poor decision-making in these patients.
Parkinson’s disease is widely recognised for its motor symptoms, including tremors, stiffness, and slowed movements. However, many patients also experience non-motor challenges such as apathy and an inability to feel pleasure, conditions that are linked to a deficiency of dopamine, a neurotransmitter often referred to as the "feel-good" hormone.
The study focused on how Parkinson’s patients process reward stimuli that typically trigger dopamine release and activate learning and motivational systems in the brain. Using electroencephalography (EEG), the researchers measured brain activity in 28 Parkinson’s patients and 28 healthy individuals as they performed reward-based learning tasks. The EEG data were recorded before and after the patients took dopamine medication.
Findings revealed that Parkinson’s patients showed significantly weaker "reward positivity" signals—a brain response associated with recognising and responding to rewards. This weakened signal suggests that the brain’s reward-processing circuits are impaired in Parkinson’s, limiting patients’ ability to engage in motivated or goal-directed behaviour.
Importantly, dopamine medication, while effective in easing motor symptoms, failed to restore normal reward positivity levels. According to lead researcher Prof. Nivethida Thirugnanasambandam from the Department of Biosciences and Bioengineering, this could be because medication restores dopamine levels but does not replicate the natural burst-like release required for cognitive processes.
The study also found that Parkinson’s patients had reduced theta-gamma synchronisation—brain wave patterns essential for communication between regions involved in learning and reward. Although medication partially restored this synchronisation, it was not enough to fully recover cognitive functions. This suggests that additional therapeutic approaches may be needed to address non-motor symptoms of Parkinson’s disease.
The researchers propose that theta-gamma coupling could serve as a potential biomarker for identifying cognitive impairments related to reward processing in Parkinson’s patients. The study paves the way for future research on adjunct treatments targeting these cognitive deficits.