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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 aging 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 the cellular functions as well as on the activity of neuronal networks (Hosp et al., 2017; Burgold et al., 2019; Blumenstock and Dudanova, 2020; Blumenstock et al., 2021; Riera-Tur et al., 2022). However, it is still unclear why certain populations of neurons are particularly vulnerable to degeneration, while other neurons in their vicinity remain largely intact. Moreover, we lack understanding of how the demise of the vulnerable neuronal cell types affects the functionality of neural circuits, and how these changes are linked to behavioral defects. Our goal is to identify molecular pathways and neural circuit impairments that play a role in neuronal vulnerability and could provide promising targets for new therapeutic approaches. 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.

The major current directions of our research are:

  1. Determining the role of protein quality control in neurodegeneration
  2. Deciphering cortical circuit alterations in neurodegenerative diseases
  3. Designing disease-modifying strategies