Our group focuses on deciphering molecular and circuit mechanisms of neurodegenerative disorders such as Huntington’s disease and Alzheimer’s disease.
Neurodegenerative diseases such as Alzheimer’s disease, Parkinson’s disease and Huntington’s disease are age-dependent, so far incurable disorders that are becoming increasingly prevalent in our society. At the cellular level, these diseases are characterized by progressive dysfunction and ultimate loss of neurons. Another common hallmark of neurodegenerative disorders is misfolding and aggregation of certain proteins such as Aβ, Tau, α-synuclein or mutant Huntingtin. Previous work from our group investigated the effects of protein aggregates on protein homeostasis (proteostasis) in neurons, as well as on the activity of neuronal networks. However, it remains unclear why certain populations of neurons are particularly vulnerable to degeneration, while other neurons in their vicinity remain largely intact; which molecular mechanisms underlie these differences in vulnerability, and how this affects the function of neural circuits. We tackle these questions with the help of cell culture and genetic mouse models, using a combination of molecular and histological approaches, behavioral analyses and in vivo imaging.
Our team is investigating pathological mechanisms of neurodegenerative diseases. Our goal is to identify molecular pathways and neural circuit defects that play a role in neuronal vulnerability and could provide targets for new therapies.