A poor understanding of the interacting risk factors for schizophrenia and other major psychiatric diseases prohibits advances in their prevention and treatment. By an interdisciplinary approach, our laboratory seeks to improve our understanding of how different environmental factors contribute to the development of neuropsychiatric disorders. Clinical studies from our laboratory support the notion that inflammatory mechanisms relating to innate immune function and activation of endogenous retroviral elements (HERV) are associated with the onset of schizophrenia. A key question is when such mechanisms are initiated.
Experimental studies from our laboratory illustrate how early-life infections (see figure) and genetic variants resulting in functional deficits in the adaptive immune response interact to promote inflammatory conditions that can contribute to the development of behavioral deficits relating to cognitive and emotional domains.
Using the unique Swedish biobanks and registers we have more recently demonstrated risk factors for serious psychiatric illnesses such as schizophrenia and autism that appear to act during early life. Such factors include maternal antibodies to both infectious and dietary antigens as well as altered levels of acute phase proteins in the neonatal blood. Register-based studies indicate that exposure to serious CNS infections during childhood also contributes to the development of non-affective psychoses later in life.