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Schizophr Bull. 2017 Oct 21;43(6):1190-1196. doi: 10.1093/schbul/sbx121.

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

Author information

1
Psychosis Studies Department, Institute of Psychiatry, Psychology and Neuroscience, King's College, London, UK.
2
National Institute for Health Research (NIHR) Mental Health Biomedical Research Centre, South London and Maudsley NHS Foundation Trust and King's College, London, UK.
3
Psychiatric Imaging Group, Clinical Science Centre, Imperial College, London, UK.

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.

KEYWORDS:

dopamine; neurodevelopment; risk factors; sociodevelopment

PMID:
28981842
PMCID:
PMC5737804
DOI:
10.1093/schbul/sbx121
[Indexed for MEDLINE]
Free PMC Article

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