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Our results add to growing evidence for the Carter effect and a multifactorial threshold model in CTEV.
We deduced two criteria that every nuclear susceptibility gene for schizophrenia should fulfill for the persistence of the disease under general assumptions of the multifactorial threshold model.
They support the 'Carter effect', suggesting CTEV develops though a multifactorial threshold model with females requiring a higher risk factor 'load', and suggest areas where future aetiological investigation might focus.
We assume the multifactorial threshold model [1], in which quantitative traits such as liability to the disease are determined by multiple genetic and non-genetic factors including a stochastic and/or an epigenetic effect.
Here we deduce two criteria that a nuclear susceptibility gene for SZ should fulfill for the persistence of the disease under general assumptions of multifactorial threshold model, and present their implications for genetic association studies and genetic models for SZ using the epidemiological data in a large-sampled Finish cohort study.
External (to the case control data) epidemiological information on disease prevalence is required if the multifactorial threshold model is to be used to calculate locus-specific heritabilities.
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The current understanding of the origin of schizophrenia is mainly based on the multifactorial-threshold (MFT) model of genetic liability and the neurodevelopmental model [ 1].
Extended Data Fig. 6 Behaviour of the fixed threshold model.
Models of diffusion in social networks: we review the independent cascade model and the threshold model.
Existing evaluations used a sire threshold model.
Larkin and Paton are describing the dynamics of Granovetter's threshold model of group behavior.
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