Henna Jäntti


I want to understand how glia-neuron interaction can trigger cognitive dysfunction in diseases like schizophrenia and Alzheimer’s disease. I completed a PhD in neuroinflammation at the University of Eastern Finland in Tarja Malm’s lab. There I established a method to differentiate human stem cell derived microglia and showed that genetic and environmental risk factors for Alzheimer’s disease alter microglial functions. I also discovered that a novel mechanosensitive receptor modulates the disease relevant functions of microglia. Intriguingly, all these approaches pointed towards metabolic dysregulation in microglia, suggesting a common cellular processes both for genetic and environmental risks. There are indications that these processes that can go awry in early stages of Alzheimer’s are also altered in schizophrenia. In both diseases, synaptic dysfunction is observed in hippocampus and prefrontal cortex. Now at the Stevens lab, my postdoctoral work focuses on setting up more complex coculture systems that include also human neurons and astrocytes in addition to microglia. My aim is to uncover molecular mechanisms of glia-neuron interactions underlying synaptic dysregulation using human cells with gene variants associated to Schizophrenia risk.