Morphogenesis and Differentiation Program
Panum, Bygning: 18.4.12
2200 København N
By in vitro studies we try to approach fundamental unit operations in neuroinflammation and neurodegenerative disease with the aim of obtaining mechanistic insight.
The lab has a long-standing interest in NADPH oxidase (NOX2) trafficking and function in microglia (glia and macrophage cell of the CNS), and we would like to analyze in depth the molecular composition and function of the agonist-regulated secretory vesicles containing NADPH oxidase that we have identified.
By an exemplifying article we have recently introduced and substantiated the idea that proteotoxic a-synuclein aggregates, and in a wider perspective other amyloid species, are secreted from neurons by exophagy; the exocytosis of autophagosomes. Current work is aimed at understanding the bifurcature in the autophagsomal pathway, leading to either lysosomal degradation or secretion, and the localization and role of regulatory stress kinases JNK and p38MAPK.
Most recently we have shown that inflammatory, but not resting, microglia upregulate the secretion of a-synuclein species from dopaminergic neuron cell models through mechanisms that require microglia cytokine secretion and stimulation of neuronal stress kinases JNK2 and JNK3
- NADPH Oxidase trafficking and function in microglia
- Stress kinases in a-synuclein autophagy and secretion from parkinsonergic neurons
- Uptake and processing of tau by microglia
- Synaptic dysfunction in models of Huntington Disease
- Trafficking defects in models of Huntington Disease