As one might hope, progress is being made in multiple ways. The field that is moving downward – in a reductionist sense – to more detailed biological mechanisms at the DNA, RNA, and protein levels. These efforts are being driven by rapid technological advances. However, we are straining to develop the conceptual and analytic tools to keep pace with the information generated by these new generation technologies. Inhibitors,research,lifescience,medical At the same time, the field is moving out into the environment

to clarify the often critical inter-relationship between these two broad classes of risk factors. Equally importantly, it is moving “forward” in emphasizing the importance of time and development. This can all be confusing and sometimes a bit overwhelming. In a desire to simplify, some, in the “glow” of the new biological tools now available, have devalued the genetic epidemiologic approaches. These approaches, Inhibitors,research,lifescience,medical they suggest, focus on “statistics” but not “real genes.” However, knowledge gained from genetic epidemiology, in addition to provide a guiding light for molecular approaches, also have their own inherent validity. Studying aggregate genetic risk factors allows Inhibitors,research,lifescience,medical us to build etiologic models that can inform prevention efforts, aid policy makers in planning for research programs, and provide critical input

into revisions of psychiatric nosology. We would like to close by emphasizing that knowledge about the role of genetic factors in the etiology of psychiatric illness can be profitably understood from several perspectives. The human mind/brain system Inhibitors,research,lifescience,medical – the organ that

instantiates psychiatric illness – is AZD4547 in vitro surely influenced by processes occurring at the levels of basic molecular biology, neural systems and networks, and psychological, social, and cultural processes.185 A full understanding of the processes whereby Inhibitors,research,lifescience,medical genetic risks lead to the development of psychiatric disorders will surely require considering all these perspectives, each of which contributes a useful viewpoint with methodologies that have important (and different) strengths and limitations. Contributor Information Danielle M. Dick, Virginia Institute of Psychiatric and Behavioral Genetics; Thymidine kinase Department of Psychiatry; Department of Human and Molecular Genetics, Virginia Commonwealth University School of Medicine, Richmond, VA, USA. Department of Psychology, Virginia Commonwealth University, Richmond, Virginia, USA **
For more than 10 years, genome research has focused on finding genetic risk factors for common disorders, based on the “common disease – common variant (CDCV)” hypothesis – the intuitive but unproven assumption that for most of the common disorders like dementia, diabetes, coronary heart disease, autism, and hypertension, there are common genetic risk factors.