Rationale for the research area
Neuroinflammation, normally a transient neuroprotective state, can transform into a chronic state in which the inflammation becomes self-propagating and can progress to neurodegeneration. Recent studies suggest that neuroinflammation is an early or even a causative event in the development of Alzheimer's and Parkinson's diseases. Neuroinflammation is a brain-specific response to a variety of cues including exposure to environmental pollutants that normally protects or repairs brain cells, but which under certain circumstances can switch to induce neurodegeneration. The mechanism underlying the switch from protective/reparative to pro-degenerative function is not well understood.
This research area utilizes in vitro models to identify and characterise key events leading to the switch of neuroinflammatory state from neuroprotective to neurodegenerative. In particular, the focus is on passage through the blood-brain barrier and metabolic reprogramming of brain cells occurring during the inflammatory process. Early changes in proteins and metabolite levels linked to changes in brain cell metabolism will be evaluated for their utility as early markers of toxicity, with the ultimate goal of measuring them in human biological fluids.
The identification of human biomarkers of neuroinflammation that can be measured in biological fluids could aid in assessing onset of potentially neurodegenerative inflammation. Furthermore, the obtained data will be used for the development of Adverse Outcome Pathways (AOPs), that will be useful for risk assessment and finally for regulatory purposes.