Research Area
Aging

Grant Type
Fellowship

Year
2020

Abstract

The changes to social cognition that occur in frontotemporal dementia (FTD) are some of the earliest, most disruptive, and least treatable manifestations of the disease. While social attachment deficits and loss of empathy are characteristic and diagnostic of FTD, increased social withdrawal and isolation occur across many neurodegenerative disorders, including Alzheimer’s disease and related disorders. In fact, social isolation is not only thought of as a potential symptom, but increasingly recognized as an important risk factor for dementia and other age-related diseases. Yet, surprisingly, we understand very little about the basic neurobiology of social attachment and how disease disrupts this essential human behavior.

I aim to develop a novel model system for understanding social attachment deficits in dementia using the prairie vole, one of the few species that forms long term adult attachments. Using molecular genetic approaches developed in the vole, I have targeted high confidence risk genes associated with FTD to understand how mutations in these genes impact activity in specific neural circuits and ultimately lead to deficits in attachment behavior. This approach will provide a window into the neural mechanisms underlying the distinct behavioral changes seen in patients, particularly as many of the brain regions and molecular pathways are likely to be shared across species. Having such a model organism may permit the rational design and testing of therapeutic approaches to ameliorate the breakdown of social attachments in patients with age-related neuropsychiatric diseases.