Investigating the neurodevelopmental hypothesis of schizophrenia.
1. An optimal intra-uterine environment is critical for normal development of the brain. It is now thought that abnormal development in a compromised prenatal and/or early postnatal environment may be a risk factor for several neurological disorders that manifest postnatally, such as cerebral palsy, schizophrenia and epilepsy. 2. The present review examines some of the effects of abnormal prenatal brain development and focuses on one disorder that has been hypothesized to have, at least in part, an early neurodevelopmental aetiology: schizophrenia. 3. The key neuropathological alterations and changes in some of the neurotransmitter systems observed in patients with schizophrenia are reviewed. Evidence in support of a neurodevelopmental hypothesis for schizophrenia is examined. 4. A summary of the animal models that have been used by researchers in an attempt to elucidate the origins of this disorder is presented. Although no animal model of a complex human disorder is ever likely to emulate deficits in all aspects of structure and function observed in patients with a neuropsychiatric illness, our findings and those of others give support to the early neurodevelopmental hypothesis. 5. Thus, it is possible that an adverse event in utero disrupts normal brain development and creates a vulnerability of the brain that predisposes an already at-risk individual (e.g. genetic inheritance) to develop the disorder later in life.
Rehn
Alexandra E
AE
Department of Anatomy and Cell Biology, The University of Melbourne, Parkville, Victoria, Australia.
Rees
Sandra M
SM
D000818:Animals; D001921:Brain / Q000002:abnormalities* / Q000196:embryology / Q000378:metabolism; D004195:Disease Models, Animal; D006801:Humans; D018377:Neurotransmitter Agents / Q000378:metabolism; D012307:Risk Factors; D012559:Schizophrenia / Q000503:physiopathology*
D018377:Neurotransmitter Agents