| Apathy concerns a quantitative reduction of voluntary, goal-directed behaviors that impairs daily functioning. It is a prominent and severely debilitating aspect of several psychiatric disorders, most notably schizophrenia. Little is known regarding the neuroscientific basis of these symptoms, however. Clinically, it has been suggested that two forms of apathy can be distinguished: cognitive apathy (CA) and social-emotional apathy (SEA). Both involve a reduced behavioral activation. However, I propose that CA is primarily a dysfunction of cognitive control and self-initiated action, whereas SEA is primarily a failure to signal the salience of positive events (and hence reduced motivation). The present project, for the first time, tests the hypothesis that two neuroanatomically distinct routes underlie these two forms of apathy in schizophrenia: a dorsal frontostriatal circuit including the right parietal cortex for CA and a more ventral frontostriatal circuit including the reward system for SEA. The objective of this project is threefold. First, to investigate the differential cognitive and neural basis of apathy in schizophrenia patients, using functional MRI. Second, we will test the hypothesis that CA is associated with poorer long-term functioning and neurocognitive deficits. Third, we will conduct a controlled treatment study of a novel intervention to improve CA: transcranial magnetic stimulation over the right dorsolateral prefrontal cortex to activate a frontostriatal-parietal network. In summary, the present proposal aims to elucidate fundamental cognitive and emotional processes underlying apathy. A distinct contribution will be made by unravelling the neural basis of two pathways that may lead to apathy. Last but not least, the treatment study may contribute to novel strategies that will ultimately improve patients' lives. Ultimately, the results will also have implications for understanding apathy in patients with depression, brain damage and neurodegenerative diseases. |
