Summary
Frontotemporal dementia (FTD) is a progressive neurodegenerative disorder that causes severe personality and behavior changes. A hexanucleotide repeat expansion in the C9orf72 gene is FTD's most common genetic cause. I aim to elucidate the mechanisms of circuit dysfunction in C9orf72-FTD, focusing on understanding the relationship between cortical hyperactivity, the progression of C9orf72 hexanucleotide repeat pathology, and behavior. Understanding these aspects is crucial for developing effective and timely treatments for FTD. The first aim of this research is to monitor the progression of ne
