Mary Patton, PhD, an assistant professor in the Department of Anatomy and Neurobiology at the University of Tennessee Health Science Center, has received a $747,000 grant from the National Institute of Mental Health to study why people with certain mental illnesses lose motivation and how that can be treated.
The project focuses on a common and deeply disruptive symptom seen in schizophrenia and other psychiatric conditions: amotivation, or the inability to start or sustain goal-directed activities. This symptom can greatly affect daily functioning and quality of life, yet treatments for it remain limited.
Dr. Patton’s work will explore how a specific, and surprising, brain pathway may be involved in amotivation. Using advanced tools and a well-established genetic model linked to schizophrenia (22q11 deletion syndrome), her research will examine the interaction between two key brain regions, the thalamus and the dorsal striatum, areas that are more commonly involved in sensory and motor learning.
Preliminary studies suggest that communication between these brain regions breaks down in the model, and that a special type of brain cell called a cholinergic interneuron may be overactive and contributing to this disruption. Remarkably, early findings show that when this altered communication is generated in control subjects, amotivation occurs. It is possible that when this overactivity is blocked, the brain’s communication will improve, and motivation may return.
With this funding, Dr. Patton’s research aims to pinpoint how certain brain cells influence motivation. It will also seek to understand how faulty brain signaling develops and to identify the specific brain circuits involved.
Her findings could lead to entirely new ways to restore motivation in people with schizophrenia, depression, addiction, and other disorders where altered motivation occurs.
“This work has the potential to reshape how we think about and treat amotivation in mental illness,” Dr. Patton said. “Understanding the brain’s motivation circuits could open the door to better, more targeted therapies.”