Why schizophrenia epidemiology needs neurobiology--and vice versa.
Schizophrenia epidemiology can provide us with valuable information to guide research directions. However, while epidemiology is useful for generating candidate risk factors, it can not always deliver studies that prove causality. We argue that the field needs more translational research that links schizophrenia epidemiology with molecular, cellular, and behavioral neuroscience. Cross-disciplinary projects related to candidate genetic or nongenetic risk factors not only can address the biological plausibility of these factors, but they can serve as catalysts for discovery in neuroscience. This type of cross disciplinary research is likely to be more efficient compared to clinically dislocated basic neuroscience. Examples of this type of translational research are provided based on (a) the impact of prenatal nutrition and prenatal infection on brain development and (b) understanding the causes and consequences of agenesis of the corpus callosum. We need to build shared discovery platforms that encourage greater cross-fertilization between schizophrenia epidemiology and basic neuroscience research.
McGrath
John J
JJ
Queensland Centre for Mental Health Research, The Park Centre for Mental Health, Wacol, Queensland 4076, Australia. john_mcgrath@qcmhr.uq.edu.au
Richards
Linda J
LJ
D055673:Acrocallosal Syndrome / Q000453:epidemiology / Q000235:genetics / Q000503:physiopathology; D001921:Brain / Q000503:physiopathology*; D015984:Causality; D003299:Cooperative Behavior; D005260:Female; D020022:Genetic Predisposition to Disease / Q000235:genetics; D006801:Humans; D007231:Infant, Newborn; D033183:Interdisciplinary Communication; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000453:epidemiology / Q000235:genetics / Q000503:physiopathology; D012106:Research; D012307:Risk Factors; D012559:Schizophrenia / Q000453:epidemiology* / Q000235:genetics / Q000503:physiopathology*