Ana Osorio Oliveira
(Postdoctoral Researcher at Karolinska Institute)
Ana Osório Oliveira has been a postdoctoral Researcher at Karolinska Institute since 2019. Her interests are focused on the understanding of the molecular mechanisms which lead to neurodegeneration in diseases such as Alzheimer's, Parkinson's and Huntington's diseases. These diseases are intimately associated with protein misfolding and aggregation in specific regions of the brain, therefore she is very interested in studying the toxicity caused by these abnormal proteins in the brain. In addition, she is determined on understanding how glial cells affect brain function in health, aging and disease, and to develop novel therapeutic strategies that target glial cells to prevent, reverse or slow diverse neuropathologies. Ana is also passionate about science communication & education, driving innovative research, mentoring students and forming multidisciplinary and diverse collaborations. Ana has done her PhD at the Gladstone Institutes - University of California San Francisco and University of Lisbon. Before joining Karolinska, Ana was a Postdoctoral researcher and a BioScience Career Ambassador at Stanford University.
Progress in iPSC-based cellular systems provides new insights into human brain development and early neurodevelopmental deviations in psychiatric disorders. Among these, studies on schizophrenia (SCZ) take a crucial role owing to its high heritability and multifarious evidence that it evolves from a genetically induced vulnerability in brain development. Recent iPSC studies on patients with SCZ indicate that functional impairments of neural progenitor cells in monolayer culture extend to brain organoids by disrupting neocorticogenesis in an in vitro model. Our laboratory observed differences in microgliamediated engulfment of neuronal synapses in vitro between healthy controls and patients with SCZ. In addition, the formation of hippocampal circuit-like structures in vitro is impaired in patients with SCZ as is the case for glia development. Intriguingly, chimeric-mice studies show altered oligodendrocyte and astrocyte development in vivo that highlights the importance of cell-cell interactions in the pathogenesis of early-onset SCZ. These alterations are associated with behavioral and emotional impairments mimicking those of patients. As astrocytes guide neuronal maturation, this research too highlights the significance of cell–cell interactions in the pathogenesis of SCZ. Likewise, cortical imbalances in excitatory-inhibitory signaling may result from a cell-autonomous defect in cortical development. Overall, several findings indicate that genetic risk in SCZ impacts neocorticogenesis, hippocampal circuit formation, and the development of distinct glial and neuronal subtypes. Our research focus on emerging evidence regarding perturbed glia development, namely microglia and astrocytes reactivity in patients with SCZ.