Ebru Ercan-Herbst

Unraveling the untapped pathology of schizophrenia: Hypomyelination

Abstract

Schizophrenia is a neurodevelopmental disorder that affects about 1% of the population globally. Despite its high prevalence, the causes of the onset of the disorder remain unknown. Current evidences underline reduction in myelin integrity in the white matter tracts of schizophrenia patients, highlighting a contribution of myelination in the development of the disease.

Myelination occurs postnatally and continues until early adulthood which coincides with the pathogenesis of schizophrenia. Myelin changes shape the neuronal circuit function, thus myelin disruption may contribute to the reduced connectivity between brain regions that has been observed in schizophrenia. Therefore, gaining mechanistic insights into the role of myelination in schizophrenia is very important to select an alternative pathway to treat this disorder.

To unravel the hypomyelination pathology of schizophrenia, we explore differentially expressed genes in neurons and oligodendrocytes from brains of schizophrenia patients and healthy controls and as well in iPSC-derived oligodendrocyte lineage cells from schizophrenia patients with hypomyelination pathology and healthy controls. To study the selected candidate targets for their role in myelination, we utilize our established 3D culture platforms of iPSC-derived oligodendrocyte lineage cells and neurons.

Biography

Dr. Ercan-Herbst primarily focuses her research on investigating neuron-oligodendrocyte interactions and identifying the molecular mechanisms underlying myelination deficits. During her postdoctoral studies at Harvard Medical School, her work centered around autism spectrum disorders, where she discovered a neuronal factor that hinders oligodendrocyte development, leading to deficits in myelination.

Over the past four years, Dr. Ercan-Herbst has been leading a team of scientists at the BioMed X Institute in Heidelberg. Her research revolves around exploring early intervention strategies for schizophrenia, with a specific emphasis on the hypomyelination pathology. In pursuit of these goals, her team develops physiologically-relevant in vivo and in vitro platforms. They also employ transcriptomics analysis on post-mortem brain samples to identify potential factors contributing to hypomyelination pathology of schizophrenia.