Abstract
The current schizophrenia concept is built on experts' agreement on the matter, and it is basically rooted in the epidemiological and clinical evidence. However, the numerous and intensive attempts to find the biological underpinnings of this syndrome face almost constantly a low degree of replication of the results. We have reviewed previously published work to contribute to identify some reasons underlying that failure. The difficulty in replicating biological findings in schizophrenia may relate to the intrinsic heterogeneity among patient samples, acquired through the current diagnostic criteria. As a result, the necessary replication for any finding to be accepted as characteristic data for schizophrenia would be impeded. Therefore, a new frame based on identification of correlates of the most replicated biological anomalies in schizophrenia to date may contribute to overcome those difficulties.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Antipsychotic Agents / therapeutic use
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Brain / drug effects
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Brain / physiopathology
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DNA Copy Number Variations / genetics
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DNA Mutational Analysis
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Displacement, Psychological
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Dopamine / physiology
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Genetic Predisposition to Disease / genetics
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Humans
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Interpersonal Relations
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Mental Processes / drug effects
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Mental Processes / physiology
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Nerve Net / drug effects
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Nerve Net / physiopathology
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Neural Inhibition / drug effects
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Neural Inhibition / physiology
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Psychophysiology
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Receptors, N-Methyl-D-Aspartate / drug effects
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Receptors, N-Methyl-D-Aspartate / physiology
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Reproducibility of Results
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Research
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Schizophrenia / classification
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Schizophrenia / diagnosis*
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Schizophrenia / drug therapy
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Schizophrenia / physiopathology*
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Schizophrenic Psychology*
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Synaptic Transmission / drug effects
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Synaptic Transmission / physiology
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Treatment Outcome
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gamma-Aminobutyric Acid / physiology
Substances
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Antipsychotic Agents
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Receptors, N-Methyl-D-Aspartate
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gamma-Aminobutyric Acid
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Dopamine