向井 淳

  The major purpose of my work is the elucidation of the cellular and molecular pathology underlying susceptibility to schizophrenia with the long-term goal being the design of more targeted, and therefore more effective treatments. I am accomplishing my goal by analyzing a series of mouse strains that are models either for individual genes or clusters of genes that human genetic studies have identified as significantly associated with schizophrenia, especially the 22q11.2 and SETD1A loci. I hope to elucidate how neuronal networks in or between the frontal cortex as well as hippocampus produce cognitive functions and how these functions are compromised in schizophrenia aiding to the understanding of the specifics of behavioral deficits seen in SCZ, as emerged by cortical and hippocampal network dysfunction. My work focuses in understanding the mechanisms underlying anatomical and functional brain dysconnectivity arising as a result of the 22q11 micro deletion and/or ultra-rare coding variants (URVs), such as SETD1A. My extensive scientific and clinical experiences leave me well-suited to lead the proposed project.

   These studies promise to identify a set of disease-specific genomic targets and provide new insights into presymptomatic diagnosis and early therapeutic intervention, in the context of the new field of Precision Psychiatry.