The group investigates the role that astrocytes play in neurodegenerative diseases. To be able to design effective therapeutic strategies for neurodegenerative disorders such as Alzheimer's disease, we need to investigate not only how neurons become dysfunctional but also to better understand what is the contribution of glial cells to the degeneration of neurons and the disease progression.
In Alzheimer’s disease, as in many other neurodegenerative diseases, deposition of misfolded proteins is a hallmark of the disease. Alterations in protein homeostasis contribute to the deposition of β-amyloid peptide in extracellular plaques and to the aggregation of phosphorylated tau protein in intraneuronal neurofibrillary tangles (NFTs). Protein homeostasis systems in cells include autophagy, the ubiquitin-proteasome system and chaperones. Molecular chaperones are essential to assist protein folding and to prevent accumulation of misfolded proteins. Research in the lab is studying chaperones as molecular targets to prevent Alzheimer’s disease in the context of astrocyte-neuron communication.
To explore mechanisms of astrocyte-neuron communication and its relevance to neurodegenerative diseases.
To investigate how astrocytes maintain neuronal protein homeostasis in Alzheimer’s disease and how chaperones can mediate this protection.
Our research is funded by