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30 Years on: How the Neurodevelopmental Hypothesis of Schizophrenia Morphed into the Developmental Risk Factor Model of Psychosis

Research output: Contribution to journalArticle

Original languageEnglish
Pages (from-to)1190-1196
Number of pages7
JournalSchizophrenia Bulletin
Volume43
Issue number6
DOIs
StateE-pub ahead of print - 14 Nov 2017

King's Authors

Abstract

At its re-birth 30 years ago, the neurodevelopment hypothesis of schizophrenia focussed on aberrant genes and early neural hazards, but then it grew to include ideas concerning aberrant synaptic pruning in adolescence. The hypothesis had its own stormy development and it endured some difficult teenage years when a resurgence of interest in neurodegeneration threatened its survival. In early adult life, it over-reached itself with some reductionists claiming that schizophrenia was simply a neurodevelopmental disease. However, by age 30, the hypothesis has matured sufficiently to incorporated childhood and adult adversity, urban living and migration, as well as heavy cannabis use, as important risk factors. Thus, it morphed into the developmental risk factor model of psychosis and integrated new evidence concerning dysregulated striatal dopamine as the final step on the pathway linking risk factors to psychotic symptoms.

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