Abstract

Neurodevelopmental and neurodegenerative theories may be viewed as incompatible accounts that compete to explain the pathogenesis of schizophrenia. However, it is possible that neurodevelopmental and neurodegenerative processes could both reflect common underlying causal mechanisms. We hypothesized that cognitive dysfunction would gradually deteriorate over time in schizophrenia and the degree of this deterioration in adulthood would be predicted by an infant measure of neurodevelopment. We aimed to examine the association between age of learning to stand in infancy and deterioration of cognitive function in adulthood. Participants were nonpsychotic control subjects (n = 76) and participants with schizophrenia (n = 36) drawn from the Northern Finland 1966 Birth Cohort study. The schizophrenia group showed greater deterioration in abstraction with memory than controls, but there were no differences between schizophrenia and controls in rate of change of other cognitive measures. Age of learning to stand in infancy significantly inversely predicted later deterioration of abstraction with memory in adult schizophrenia (later infant development linked to greater subsequent cognitive deterioration during adulthood), possibly suggesting a link between abnormal neurodevelopmental and neurodegenerative processes in schizophrenia.

Highlights

  • Delayed motor development may reflect aberrant functional maturation of cortical-subcortical circuits, as motor delay predicts behavioral problems in later childhood and adolescence[5] and development of higher cognitive function, educational achievements, and brain structure in adulthood.[6,7,8]. Consistent with this line of research, longitudinal studies have revealed that individuals who subsequently developed schizophrenia manifested cognitive deficits, including executive dysfunction, before the onset of the illness,[1,9,10,11] suggesting that abnormal neurodevelopment is a critical part of the pathogenesis of schizophrenia.[12,13]

  • Control subjects and participants with schizophrenia were drawn from the Northern Finland 1966 Birth Cohort study, which is based on 12 068 pregnant women and their 12 058 children born alive in the provinces of Lapland and Oulu, with an expected delivery date during 1966

  • The Faculty of Medicine Ethics Committee of the University of Oulu continuously reviews the design of the Northern Finland 1966 Birth Cohort study

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Summary

Introduction

Several general population-based cohort studies have demonstrated significant associations between delay of infant motor development and the later onset of schizophrenia.[1,2,3,4] Delayed motor development may reflect aberrant functional maturation of cortical-subcortical circuits, as motor delay predicts behavioral problems in later childhood and adolescence[5] and development of higher cognitive function, educational achievements, and brain structure in adulthood.[6,7,8] Consistent with this line of research, longitudinal studies have revealed that individuals who subsequently developed schizophrenia manifested cognitive deficits, including executive dysfunction, before the onset of the illness,[1,9,10,11] suggesting that abnormal neurodevelopment is a critical part of the pathogenesis of schizophrenia.[12,13]Another conceptualization of schizophrenia is that it is a disorder with a significant neurodegenerative component.[14]. Several general population-based cohort studies have demonstrated significant associations between delay of infant motor development and the later onset of schizophrenia.[1,2,3,4] Delayed motor development may reflect aberrant functional maturation of cortical-subcortical circuits, as motor delay predicts behavioral problems in later childhood and adolescence[5] and development of higher cognitive function, educational achievements, and brain structure in adulthood.[6,7,8] Consistent with this line of research, longitudinal studies have revealed that individuals who subsequently developed schizophrenia manifested cognitive deficits, including executive dysfunction, before the onset of the illness,[1,9,10,11] suggesting that abnormal neurodevelopment is a critical part of the pathogenesis of schizophrenia.[12,13]. The same genetic, in utero, or perinatal factors that cause abnormal neurodevelopment in schizophrenia could, conceivably, cause increased degenerative processes later in the course of illness.[21]

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