Cerebral Ischemia-on-a-Chip - Investigating neuronal responses to hypoxia and treatment
Eva Voogd is a PhD student in the Department of Clinical Neurophysiology. (Co)Promotors are prof.dr. J. Hofmeijer and dr. M. Frega from the Faculty of Science & Technology.
Understanding the mechanisms of neuronal network activity under hypoxic stress is crucial for unraveling the complexities of cerebral ischemia and identifying new treatment targets. In my dissertation, I investigated how hypoxia impacts neuronal functionality in human- and rat-derived neuronal networks cultured on micro-electrode arrays (MEAs) and explored potential treatments to mitigate hypoxia-induced damage.
My findings demonstrate that both human and rat neuronal networks exhibit vulnerability to hypoxia, showing impaired activity and decreased cell viability. Notably, I discovered that stimulation of neuronal network activity during hypoxic exposure improves post-hypoxia network recovery, suggesting a potential neuroprotective mechanism. Additionally, I found that cooling neuronal networks during hypoxia preserves functionality, supporting its role as a therapeutic strategy to minimize hypoxic damage.
These results provide insights into how neuronal networks respond to oxygen deprivation and highlight the translational potential of MEA technology in modeling hypoxia-related disorders. By leveraging human-derived neuronal networks, this dissertation paves the way for future in vitro investigations of hypoxia-induced pathophysiology and offers a platform for screening potential neuroprotective interventions.
Further research should explore the molecular underpinnings of these protective mechanisms and assess how targeted pharmacological treatments may enhance neuronal network recovery post-hypoxia. This work establishes human in vitro models on MEA as valuable tools for studying neuronal network dysfunction and contributes to advancing therapeutic approaches for hypoxia-related brain injuries.
