Research summary
Neurodevelopmental and genetic studies of schizophrenia and related neuroimaging organise this corpus. The 1987 Archives of General Psychiatry paper synthesises evidence of non-specific histopathology in the limbic system, diencephalon, and prefrontal cortex of schizophrenia, arguing that the pathology arises early in development and the causative process is inactive long before clinical onset; the model is one in which an early fixed lesion interacts with normal maturational events to produce symptoms [1]. The 1986 Archives paper measured regional cerebral blood flow (rCBF) by xenon-133 inhalation in 20 medication-free chronic schizophrenia patients and 25 controls at rest, during the Wisconsin Card Sort (a DLPFC-specific task), and during a number-matching control task, finding reduced relative resting DLPFC rCBF in patients and both absolute and relative DLPFC rCBF reductions during the WCS but not during NM [6]. The 2001 PNAS COMT Val108/158 Met paper related the common functional polymorphism (which accounts for a 4-fold variation in dopamine catabolism) to prefrontally mediated cognition and prefrontal cortical physiology, providing a mechanistic link between a schizophrenia-susceptibility gene and prefrontal-dopamine regulation [2]. The 2002 Science paper on serotonin-transporter genetic variation showed that the SLC6A4 5-HTTLPR short allele, associated with reduced 5-HTT expression and function, alters human amygdala responses to fearful stimuli, providing a neural-systems-level intermediate phenotype between gene variation and anxiety traits [3]. The 2005 American Journal of Psychiatry consensus paper proposes criteria for remission in schizophrenia, motivated by the success of analogous standards in mood disorders, to give clarity to treatment goals and a common framework for trial design and effectiveness evaluation [4]. The 2008 MATRICS Consensus Cognitive Battery paper describes selection, reliability, and validity of a 36-test consensus cognitive battery for schizophrenia clinical trials, drawing on evaluation of >90 candidate tests across seven cognitive domains by the MATRICS Neurocognition Committee [5]. The six works together build a coherent programme: a neurodevelopmental conceptual frame [1], DLPFC physiology [6], susceptibility-gene mechanisms (COMT, 5-HTT) for cognition and affect [2,3], and trial-relevant consensus instruments for remission and cognition [4,5].
Recent publications
- The BDNF val66met Polymorphism Affects Activity-Dependent Secretion of BDNF and Human Memory and Hippocampal FunctionDOI
- Implications of Normal Brain Development for the Pathogenesis of SchizophreniaDOI
- Effect of COMT Val 108/158 Met genotype on frontal lobe function and risk for schizophreniaDOI
- Serotonin Transporter Genetic Variation and the Response of the Human AmygdalaDOI
- Remission in Schizophrenia: Proposed Criteria and Rationale for ConsensusDOI
- The MATRICS Consensus Cognitive Battery, Part 1: Test Selection, Reliability, and ValidityDOI
- Spatio-temporal transcriptome of the human brainDOI
- Schizophrenia genes, gene expression, and neuropathology: on the matter of their convergenceDOI
- Physiologic Dysfunction of Dorsolateral Prefrontal Cortex in SchizophreniaDOI
- 5-HTTLPR polymorphism impacts human cingulate-amygdala interactions: a genetic susceptibility mechanism for depressionDOI
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External profiles
- ORCID: https://orcid.org/0000-0003-2409-2969
- OpenAlex: openalex.org
Profile compiled from public sources (Researchmap, OpenAlex, Osaka University faculty directory). Last refreshed 2026-05. Report incorrect information.