Autism and schizophrenia are complex developmental disorders that affect approximately 1 in 100 people. Despite their high societal impact of these disorders, current therapeutic options are mostly symptom-oriented, and often provide marginal or insufficient relief to those affected. DISCONN explored how brain networks become disrupted in disorders like autism and schizophrenia. To address this question, we used cross-species brain functional neuroimaging, electrophysiology, and targeted manipulations in rodents. Understanding the roots of these networks alterations is a required step towards an improved diagnosis and treatment of complex developmental disorders.
Our research revealed general principles underlying the organization of brain network activity in the mammalian brain. Specifically, we found a general inverse relationship between the activity of one brain region, and its functional connectivity, that is, its communication with other brain areas. This observation implies that when a region is silent, its connectivity is paradoxically strengthened. In contrast, when a region is highly active, its connectivity weakens. We also demonstrated that disruptions in the function and connectivity of specific brain regions can be traced to genetic, synaptic, or developmental alterations that are relevant to the biology of autism or schizophrenia.
A major outcome of our research is the ability to link patterns of atypical brain connectivity in people with autism or schizophrenia to their biological underpinnings. This result is of crucial importance, as it may enable the use of brain imaging to identify sub-groups of autistic or schizophrenic individuals who share the same underlying biological dysfunction. In turn, this could help unpack autistic or schizophrenic populations into biologically homogeneous cohorts, paving the way to targeted precision medicine approaches.
We are currently testing this paradigm for autism stratification in partnership with within large transdiagnostic neuroimaging initiatives.
