Abstract:
Novel hypotheses of stress/vulnerability and neurodegeneration attribute schizophrenic symptoms to a hereditary predisposition.
This "vulnerability" reduces the individual's psychological threshold towards stimuli, to the point where
even minor daily stress may trigger psychotic breaks or relapses. But this is hardly the whole story.
A significant collection of somatic physiological measures (blood cortisol, autoimmunity,
lack of specific minerals), as well as certain drugs, are known to trigger symptoms
which disguise themselves as mental illness. This increases the potential for clinical misdiagnosis.

We attempt to model the neurodegenerative process in schizophrenia on several levels of neural complexity,
building upon such neural vulnerability and dysregulation hypotheses. A bifurcation analysis of the model's
dynamics offers a promising quantitative set-up and could be the key to understanding the disease process.