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RESEARCH PRODUCT

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

Vishal BhavsarRobin M. MurrayRobin M. MurrayGiada TripoliOliver D. HowesOliver D. Howes

subject

Striatal dopaminePsychosismedicine.medical_specialtyDopamineSynaptic pruningDiseaseHistory 21st CenturyRisk factor model03 medical and health sciences0302 clinical medicinesociodevelopmentmedicineHumansrisk factorsPsychiatryUrban livingPsychiatryneurodevelopmentdopamine neurodevelopment risk factors sociodevelopment Dopamine History 20th Century History 21st Century Humans Psychiatry Psychotic Disorders SchizophreniaHistory 20th Centurymedicine.disease030227 psychiatryPsychiatry and Mental healthAdult lifemedicine.anatomical_structurePsychotic DisordersSchizophreniaSchizophreniadopaminePsychology030217 neurology & neurosurgeryRegular ArticlesClinical psychology

description

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.

10.1093/schbul/sbx121http://hdl.handle.net/10447/533272