Abstract
Patients with Parkinson’s disease are impaired at incremental reward-based learning. It is typically assumed that this impairment reflects a loss of striatal dopamine. However, many open questions remain about the nature of reward-based learning deficits in Parkinson’s disease. Recent studies have found that even simple reward-based learning tasks rely on a combination of cognitive and computational strategies, including one-shot episodic memory. These findings raise questions about how incremental learning and episodic memory contribute to decision-making in Parkinson’s disease. We tested healthy participants (n=26; 14 males and 12 females) and patients with Parkinson’s disease (n=26; 16 males and 10 females), both on and off dopamine replacement medication, on a task designed to differentiate between the contributions of incremental learning and episodic memory to reward-based learning and decision-making. We found that Parkinson's patients performed equally well as healthy controls when using episodic memory, but were impaired at incremental reward-based learning. Dopamine replacement medication remediated this deficit and enhanced subsequent episodic memory for the value of motivationally relevant stimuli. These results demonstrate that while Parkinson's patients are impaired at learning about reward from trial-and-error, their ability to encode memories for the value of one-shot experiences is intact.
Significance Statement Parkinson’s disease involves disruptions to the striatum and its dopaminergic inputs, leading to motor and cognitive impairment. The exact nature of the cognitive impairment is unclear. We found that individuals with Parkinson’s disease are impaired at gradual, incremental learning of value, but retain the ability to rapidly learn value based on a single event, referred to as episodic memory. Dopamine replacement remediates the incremental learning impairments while enhancing episodic memory. These findings shed light on the extent to which different forms of memory are impacted by dopamine loss in Parkinson’s disease.
Footnotes
The authors report no competing interests
↵†These authors contributed equally to this work.