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Research Agenda for Schizophrenia 

Research Agenda for Schizophrenia
Chapter:
Research Agenda for Schizophrenia
DOI:
10.1093/9780195173642.003.0009
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date: 15 August 2018

We have learned a great deal about the early course of schizophrenia during the past two decades, leading to therapeutic optimism. However, several key areas of research continue to be a priority. First, we need to identify specific clinical characteristics in the premorbid and prodromal phases that can help us predict the individuals at a high risk for developing psychosis. Second, we do not know how to prospectively identify the early beginnings of the psychotic illness with an adequate degree of reliability to be able to intervene early. We also need to better understand the pathways to care for these patients. Educating the public and health care providers in early signs and symptoms can reduce the delay in care. Third, we need to further clarify the clinical features in the first psychotic episode that can help us predict subsequent illness course. Finally, we need to better understand the neurodevelopmental and neurodeteriorative processes that may underlie both the emergence and the subsequent course of the first psychotic episode.

It is readily apparent that the single greatest research need regarding adolescent-onset schizophrenia is simply more studies of this form of the illness apart from its more traditional manifestations. While schizophrenia is among the most widely studied psychiatric disorder, adolescent schizophrenia is rarely examined as a clinical entity onto itself. Yet it is necessary to conduct such studies, as early-onset forms may not just reflect an enrichment of risk factors for schizophrenia or greater severity of the illness, they may in fact have their own distinct etiologies and separate ranges of severity. To determine the degree of continuity and etiological similarity between adolescent-and adult-onset schizophrenia, twin, adoption, and longitudinal studies of the early-onset form of the disease should be considered a high priority.

The study of schizophrenia can serve as a model for how adolescent schizophrenia should itself be studied. More specifically, the precursors of adolescent schizophrenia must be delineated through the examination of individuals in the premorbid stages of the illness. The most effective way to accomplish this goal may be through the use of the genetic high-risk paradigm. The ascertainment of individuals who are at the highest genetic risk for illness (e.g., children of parents with schizophrenia) would allow the collection of a sample of individuals who also have the highest likelihood of developing a severe form of illness. If adolescent schizophrenia is etiologically related to other forms of the illness and represents a more severe or genetically driven form of the disease, then such a sample would also be enriched with individuals who will develop schizophrenia during adolescence. Longitudinal studies of these individuals, beginning before adolescence and continuing throughout the period of disease risk, would allow investigtors to identify changes that signal the impending expression of latent schizophrenia susceptibility. Once detected, such features could then be compared to similar profiles of premorbid change in adult preschizophrenia to determine if any of these emergent abnormalities are specific for adolescent versus adult onset of the illness. If adolescent-onset specific changes were elucidated, these would then form the screening criteria for subsequent early intervention and, ultimately, prevention efforts for schizophrenia in adolescents.

The developments in genetics and neurobiology provide investigators with powerful new tools to extend our undertanding of the evolution of schizophrenia. Such an understanding will go beyond the current emphasis on symptomatic characterizations and will include measures of behavioral and neurobiological endophenotypic vulnerability markers. Adolescence is pivotal for brain maturation and longitudinal data are necessary to establish bridges between the phenotypic manifestations of schizophrenia and the neurobiologic substrate. It is likely that multimodal intervention methods will be shaped by such knowledge in a way that will eventually delay, ameliorate, and perhaps even thwart the devastating impact of schizophrenia.